 Neurologic Structure and Function - nodes of Ranvier allow travel of nerve  White matter – processes from cell bodies

 Stephen Jo T. Bonilla, RN, MD impulses facilitating rapid & smooth nerve  Gyri – convolutions
 Department of Surgery conduction  Fissures/Sulci – indentations
 St. Luke’s Medical Center  Central Nervous System  Cerebral Hemispheres
 Neurologic Structure and Function  Brain  Right
 Neuron  Spinal Cord - temporal & spatial relationships
 Central Nervous System  Brain - analyzes non-verbal information
- Brain Forebrain Midbrain > pattern recognition
- Spinal Cord Hindbrain > line orientation
 Peripheral Nervous System Cerebrum (Mesencephalon) > complex auditory
- Cranial Nerves (Brain stem) tones
- Spinal Nerves (Cerebral hemispheres) - communicates emotion
 Autonomic Nervous System > Pons  Cerebral Hemispheres
- Sympathetic > Meninges  Left
- Parasympathetic > Medulla oblongata - produce and understand language
 Neuron (Nerve Cell) - Dura mater - mathematical calculations
Structure - problem solving
 Cell body (soma) - Arachnoid Mater  Cerebrum
- center of cell metabolism and contains cell Cerebellum Meninges
nucleus - Pia mater - provide support and protection
 Dendrites - provide nourishment
- short, unsheathed processes that transmit > Lobes - provide blood supply
impulses to cell body *Cerebral Ventricular  Dura mater
 Axons - Frontal  Arachnoid mater
- longer, sheathed processes that transmit System  Pia mater
impulses away from cell body - Parietal  Dura Mater
 Myelin sheath - Lateral ventricles  “Hard mother”
- outer covering for axons formed by - Temporal  thick, tough, outermost membrane
nervous system support cells (oligodendroglia, - Third ventricle  endosteal dura (outer layer) forms skull
Schwann cells) - Occipital periosteum
- Nodes of Ranvier – intermittent gaps that - Fourth ventricle  meningeal dura (inner layer) coapts & forms
allow communication between nerve fibers *Insula compartments & folds (tentorium)
 Neuron (Nerve Cell) *Limbic system (Rhinencephalon)  Arachnoid Mater
Function > Basal Ganglia  “Spider web-like”
 Nerve Conduction – transmission of nerve *Reticular Formation  delicate layer, separated from dura mater by
impulses > Internal Capsule a potential space (subdural space)
 Resting potential > Commissural tracts  finger-like projections (arachnoid villi)
- voltage gradient from sodium & potassium Diencephalon which aids in CSF reabsorption into the
 Action potential > Thalamus blood stream
- stimuli cause cell membrane permeability > Hypothalamus  Subarachnoid space
& voltage change resulting to depolarization & nerve  Forebrain - where CSF circulates
impulse Cerebrum (cerebral hemispheres) - larger blood vessels which branch & pass
 Restabilization  Left & right, divided by Longitudinal through the pia mater into the brain substance to
- return to voltage / chemical gradient by fissure provide major blood supply
sodium-potassium pump (utilizing ATP)  80% of total brain weight  Pia Mater
 Saltatory conduction  Gray matter (Cortex) – nerve cell bodies  “Gentle mother”
  Innermost meningeal layer  Areas of gray matter located at the base of  Nuclei of V, VI, VII, VIII cranial nerves
 Thin, delicate membrane adhering closely to each hemisphere  Contains ascending sensory tracts and
brain & spinal cord surfaces  Caudate nucleus descending motor tracts
 Cerebrum  Putamen  Reticular formation
Lobes  Globus pallidus  Medulla Oblongata
 Frontal lobes  Regulate & integrate motor activity  Approximately 1 inch long connecting brain
 Parietal lobes originating in cerebral cortex and spinal cord
 Temporal lobes  Cerebrum  IX, X, XI, and XII cranial nerves
 Occipital lobes Internal Capsule  Motor tracts from cortex to spinal cord cross
*Homunculus  Where nerve fibers from cerebral cortex over at lower edge of medulla (spinal
 Insula converge and pass on to other parts decussation)
 Rhinencephalon  Diencephalon  “Right side of the brain controls the left side
 Frontal Lobes  Thalamus of the body, and vice versa”
 Contain motor cortex (precentral gyrus)  Hypothalamus  Contains vital centers
 Controls:  Thalamus - respiration
- motor function  Located on either side of third ventricle - heart rate
- speech  Composed of nuclei (gray matter) that act as - vomiting
- written speech center relay stations for sensation - hiccups
- mental activity  Hypothalamus  Cerebellum
- primitive reflexes inhibition  Makes up the anterior wall of 3rd ventricle  “Lesser brain”
 Parietal Lobes  Controls vital functions  Posterior to pons & connected to it by
 Principal sensory area for appreciation & - water balance cerebellar peduncles
discrimination of sensory impulses (pain, - blood pressure  Control and coordinate motor movements
touch, temperature) - sleep  Cerebral Ventricular System
 Sensory speech center - appetite  Irregularly shaped, interconnected spaces
 Temporal Lobes - body temperature within brain concerned with production &
 Auditory center (interprets sound)  Affects some emotional responses (fear, circulation of CSF
 Auditory speech center (understanding of pleasure)  Lateral Ventricles
spoken words)  Control center for pituitary function - contain major part of choroid plexus that
 Long and short memory  Midbrain (Mesencephalon) produce CSF
 Behavior  Small area between diencephalon and pons  Third ventricle
 Emotion in which 3rd and 4th cranial nerves originate - posterior to hypothalamus
 Occipital Lobes  Tectum (posteriorly)  Fourth ventricle
 Visual center (interprets vision) - relay station for sight and hearing - posterior to pons & anterior to cerebellum
 Visual speech center (ability to understand  Tegmentum (centrally)  Reticular Formation
written words) - impulses from the lower brain are  Diffuse system of nerve fibers & cells
 Insula (Central Lobes) conducted to the cortex via ascending tracts beginning in the central core of the medulla
 Deep within sylvian fissure  Cerebral peduncles (anteriorly) & lower pons
 Visceral functions - contain descending motor tracts  Reticular Activating System (RAS)
 Rhinencephalon (Limbic System)  Brain Stem - unknown precise function
 Hippocampus – long-term memories  Pons - essential for arousing from sleep &
 Amygdala – center of emotions; receives  Medulla Oblongata remaining alert
rich supply from the olfactory system  Pons - injury produces anesthesia & coma
 Cerebrum  Bridge  Spinal Cord
Basal Ganglia  Located between midbrain & medulla  Continuous with brain stem
oblongata  Structure
 - H-shaped gray matter in center surrounded  Each nerve is attached to spinal cord by two - sleep, wakefulness
by white matter roots - emotions, sexual behavior
 Function  Dorsal Root - food intake, temperature, pain
- Sensory (afferent) pathways through - receives sensory input from sensory  Histamine
ascending tracts to brain receptors throughout the body - allergic response, gastric secretions,
- Motor (efferent) pathways through  Ventral Root alertness
descending tracts from brain to nerves supplying - contains combination of motor fibers  Acetylcholine
muscles, glands & other body parts innervating glands & voluntary & involuntary - autonomic nervous system
- Reflex pathway muscles - movements
*Reflex – involuntary response to a stimulus  Spinal Nerves  Gamma Amino Butyric Acid (GABA)
 Peripheral Nervous System Spinal Nerve Plexuses - inhibitory action
 Cranial Nerves  Cervical Plexus
 Spinal Nerves - sends motor impulses to neck muscles
 Cranial Nerves - sends out phrenic nerve, activating the
I. Olfactory Se smell diaphragm
II. Optic Se vision - receives sensory impulses from neck &
III. Oculomotor Mo eye muscles back of head
IV. Trochlear Mo one eye  Brachial Plexus
muscle - innervates shoulder, arm, forearm, wrist, &
V. Trigeminal Mi sensory to head hand
& face; mastication  Lumbosacral Plexus
VI. Abducens Mo one eye - innervates lower extremities
muscle - sends out sciatic nerve
VII. Facial Mi facial muscles,  Autonomic Nervous System
sensory to tongue  Sympathetic Nervous System
VIII. Acoustic Se hearing & - originates from thoracic & lumbar areas of
balance spinal cord
IX. Glossopharyngeal Mi - accelerates some body processes in
swallowing muscles, sensory to response to stress
 Parasympathetic Nervous System
tongue & throat - originates in III, VI, IX, & X cranial
X. Vagus Mi larynx, thoracic nerves, and in sacral segment of spinal cord
& abdominal organs - balances action of sympathetic nervous
XI. Spinal Accessory Mo neck system
muscles  Neurotransmitters
XII. Hypoglossal Mo tongue muscles  Dopamine
 Spinal Nerves - movements
 8 cervical - emotions
 12 thoracic - controls acetylcholine
 5 lumbar  Norepinephrine / Epinephrine
 5 sacral - attention, learning, memory
 1 coccygeal - sleep, wakefulness
------------------- - mood
 31 pairs - autonomic nervous system
 Spinal Nerves  Neurotransmitters
 Serotonin
Neurologic Examination - apply a painful stimulus (rub the sternum) - Dysphonia – less severe impairment in
Stephen Jo T. Bonilla, RN, MD Coma volume, quality or pith of voice
Department of Surgery - apply repeated painful stimuli Aphasia
St. Luke’s Medical Center - remains unarousable w/ eyes closed Wernicke’s (receptive) Broca’s (expressive)
Neurologic Examination Posture and Motor Behavior - fluent, rapid, effortless - nonfluent, slow,
Mental Status Examination Does the px lie in bed or walks around? laborious
Cranial Nerves Note body posture and ability to relax - articulation are good but - articulation are impaired
Motor System Observe pace, range & character of movements but
Sensory System Voluntary control? sentences lack meaning words are meaningful
Cerebellar System Are certain parts immobile? - impaired word/reading - impaired repetition &
Reflexes Dress, Grooming, and Personal Hygiene writing
Mental Status Examination Grooming & personal hygiene may deteriorate in comprehension, repetition, - fair word/reading
Appearance and behavior depression, schizophrenia, & dementia naming, writing comprehension
Speech and language Excessive fastidiousness may be seen in an - posterior superior - posterior
Mood obsessive-compulsive disorder inferior frontal lobe
Thoughts and perceptions One-sided neglect may result from a lesion in the temporal lobe
Cognitive functions opposite parietal cortex, usually the non-dominant Testing for Aphasia
- Memory side Word comprehension
- Attention Facial Expression - “point to your nose”
- Information & vocabulary Observe the face, both at rest & when interacting - “point to your eye, then knee”
- Calculations with others Repetition
- Abstract thinking Are they appropriate? - “ask px to repeat a phrase (“no ifs, ands, or
- Constructional ability Anxiety, depression, apathy, anger, elation buts”)
Appearance and Behavior Facial immobility of parkinsonism Naming
Level of Consciousness Manner, Affect, and Relationship to Persons and - parts of a watch
Posture and Motor Behavior Things Reading comprehension
Dress, Grooming, and Personal Hygiene Assess the patient’s affect & its appropriateness - read a paragraph aloud
Facial Expression Blunt Writing
Manner, Affect, and Relationship to Persons and Flat - write a sentence
Things Does the patient seem to hear or see things that you Speech and Language
Level of Consciousness do not? Fluency
Alert Does the patient seem to be conversing with someone - rate, flow, melody of speech, content &
- speak to px in a normal tone of voice who is not there? use of words
- opens eyes, looks at you, responds fully & Speech and Language - hesitancy & gaps
appropriately Quantity - monotonous
Lethargy Rate - circumlocutions (phrases or sentences are
- speak in a loud voice (“How are you?”) Loudness substituted for a word the person can not think of)
- drowsy, opens eyes, looks at you, responds Articulation of words - paraphasia – words are malformed (“I
to questions and falls asleep - Dysarthria – defect in the muscular control write w/ a den”); wrong (“I write w/ a beer”); or
Level of Consciousness of speech apparatus (lips, tongue, palate or pharynx) invented (“I write w/ a zar”)
Obtundation (nasal, slurred, or indistinct) Mood
- shake the px gently as if awakening a - Aphasia – disorder in producing or Sadness
sleeper understanding language Contentment
- opens eyes, looks at you, responds slowly, - Aphonia – loss of voice accompanying Joy
& is somewhat confused disease affecting the larynx or its nerve supply Euphoria
Stupor Anger
Anxiety - digit span X Vagus Mi (S) External meatus,
Attachment - serial 7s pharynx, larynx, aortic sinus, thoracic &
Thought and Perceptions - spelling backward abdominal viscera; (M)
Thought Processes Cognitive Functions pharynx & larynx
- logic, relevance, organization, & coherence Memory (ability to register, store, & retrieve XI Accessory Mo Trapezius, SCM, muscles
Circumstantiality information) of pharynx & larynx
Derailment (Loosening of Associations) - immediate XII Hypoglossal Mo Muscles of tongue
Flight of Ideas - recent (short-term) Cranial Nerves
Neologisms - remote (long term) I: Olfactory
Blocking - retrograde, antegrade, psychogenic - present patient w/ familiar & non-irritating
Confabulation amnesia) odors (coffee, soap, vanilla)
Perseveration New Learning Ability - with eyes closed, test each nostril one at a
Echolalia Higher Cognitive Functions time & ask px to identify
Clanging Information and Vocabulary Cranial Nerves
Thought Content Calculating ability II: Optic
Compulsions Abstract thinking - inspect both optic fundus (optic disc) w/
Obsessions - proverbs ophthalmoscope
Phobias - similarities - check visual fields by confrontation test
Anxieties Constructional ability Cranial Nerves
Feelings of Unreality - ability to reproduce figures or draw a III: Oculomotor
Feelings of Depersonalization figure on command - pupillary reactions to light
Thought Content Cranial Nerve Cranial Nerves
Delusions Examination III: Oculomotor
- persecution I Olfactory Se Smell IV: Trochlear
- grandiosity II Optic Se Vision V: Abducens
- jealousy III Oculomotor Mo EOM except lateral rectus Cranial Nerves
- reference & sup oblique; pupil & ciliary muscle of lens V: Trigeminal
- being controlled IV Trochlear Mo Sup oblique muscle - Motor (palpate temporal & masseter
- somatic V Trigeminal Mi muscles while patient clenches teeth)
Perceptions Ophthalmic (S) Cornea, nasal mucous - Sensory (light touch & corneal reflex)
Illusions membrane, skin of face & scalp Cranial Nerves
Hallucinations Maxillary (S) Skin of face, VII: Facial
Insight and Judgment mucous membrane of mouth & nose, teeth - raise both eyebrows
Insight Mandibular (M) Muscles of - frown
- “what seems to be the problem?” mastication; (S) skin of face, mouth, teeth - close both eyes tightly & try opening
Judgment VI Abducens Mo Lateral rectus muscle - show both upper & lower teeth
- process of forming an opinion or VII Facial Mi (M) Muscles of - smile
evaluation about something facial expression; (S) taste (ant 2/3 of tongue); - puff out both cheeks
- “how do you plan to get the help you’ll lacrimal, Cranial Nerves
need after leaving the hospital?” submandibular & sublingual glands VIII: Vestibulo-Cochlear
Cognitive Functions VIII Vestibulo- Se Equilibrium - Hearing (Weber’s & Rinne’s test)
Orientation cochlear Hearing - specific tests of vestibular function are
- time IX Glossopharyngeal Mi (M) seldom included in the usual neuro exam
- place Stylopharyngeus muscle; (S) taste (post 1/3 of Cranial Nerves
- person tongue); pharynx; IX: Glossopharyngeal
Attention parotid gland X: Vagus
 - voice Thumb opposition (C8, T1, median nerve) - pxs arm is partially flexed at the elbow w/
- swallowing Muscle Strength (Trunk & Lower Extremities) palm down
- movements of soft palate & pharynx Flexion, extension & lateral bending of the spine - place thumb or finger firmly on biceps
- gag reflex Thoracic expansion & diaphragmatic excursion tendon
Cranial Nerves during respiration - strike w/ reflex hammer
XI: Spinal Accessory Hip flexion (L2, L3, L4—iliopsoas) - observe flexion at the elbow, & watch for
- shoulder shrug Adduction at the hips (L2, L3, L4—adductors) & feel contraction of biceps muscle
- turn head side-to-side Abduction at the hips (L4, L5, S1—gluteus medius & Reflex
Cranial Nerves minimus) Triceps (C6, C7)
XII: Hypoglossal Hip extension (S1—gluteus maximus) - flex px’s arm at the elbow, w/ palm toward
- move tongue from side to side Knee extension (L2, L3, L4—quadriceps) the body, pull it slightly across the chest
Motor System Knee flexion (L4, L5, S1, S2—hamstring) - strike the triceps tendon above the elbow
Body Position Dorsiflexion (L4, L5) - watch for contraction of the triceps muscle
- during movement & at rest Plantarflexion (S1) & elbow extension
Involuntary Movements Motor System Reflex
- tremors, tics, or fasciculations Coordination Brachioradialis or Supinator (C5, C6)
Muscle Bulk - rapid alternating movements - px’s hand should rest on the abdomen or
- compare size & contour of muscles - point-to-point movements lap, w/ the forearm partly pronated
- check for atrophy - gait - strike the radius about 1-2 inches above the
Motor System - standing & balance wrist
Muscle Tone - walk heel-to-toe - watch for flexion & supination of forearm
- feel the muscle’s resistance to passive - walk on toes & heels Reflex
stretch - hop in place Abdominal reflexes
- spasticity (increased muscle tone) - rising from sitting position - briskly stoke each side of abdomen above
- rigidity (increased resistance) Sensory System the umbilicus (T8, T9, T10), and below umbilicus
Muscle strength Superficial (T10, T11, T12)
- ask px to move actively against your Pain and temperature (spinothalamic test) - use a key, wooden end of cotton applicator,
resistance or to resist your movements Light touch (both pathways) or tongue blade
*muscle is strongest when shortest & Deep - note contraction of abdominal muscles &
weakest when longest Position and vibration (posterior columns) deviation of umbilicus toward the stimulus
Muscle Strength Grading Two-point discrimination Reflex
5 Active movement against gravity & full Stereognosis Knee (L2, L3, L4)
resistance; normal muscle strength Cerebellar System - sitting or lying down as long as the knee is
4 Active movement against gravity & some Finger-to-nose test flexed
resistance; examiner can overcome resistance Dysmetria – inability to control accurately the range - briskly tap the patellar tendon just below
3 Active movement against gravity of movement in muscle action with resultant the patella
2 Active movement of the body part when overshooting the mark (past-point) - note contraction of quadriceps with
gravity is eliminated Reflexes extension at the knee
1 Very weak muscle contraction; no active 4+ Very brisk, hyperactive,with clonus Reflex
movement 3+ Brisker than average; possibly but not Ankle (S1)
0 No muscle contraction is detectable necessarily indicative of disease - if px is sitting, dorsiflex the foot at the
Muscle Strength (Upper Extremities) 2+ Average; normal ankle
Flexion (C5, C6—biceps) 1+ Somewhat diminished; low normal - persuade the px to relax
Extension (C6, C7, C8—triceps) 0 No response - strike the Achilles tendon
Grip (C7, C8, T1) Reflexes - watch & feel for plantar flexion at the
Finger abduction (C8, T1, ulnar nerve) Biceps (C5, C6) ankle
 - if px is lying down, flex one leg at both hip
and knee & rotate it externally so that the lower leg
rests across the opposite shin
- dorsiflex the foot at the ankle & strike the
Achilles tendon
Reflex
Plantar (L5, S1)
- with an object such as key or wooden end
of applicator stick, stroke the lateral aspect of the sole
from the heel to the ball of the foot, curving medially
across the ball
- use lightest stimulus that will provoke a
response
- note movement of toes, normally flexion
Thank You.
 Neurologic Infections  Prevent, assess, and intervene for increased  Not known how they enter the bloodstream
 Stephen Jo T. Bonilla RN, MD ICP and/or hyperthermia  Bacterial Meningitis
 Department of Surgery  Ongoing assessment and documentation of Manifestations
 St. Luke’s Medical Center neurologic status  Headache
 Neurologic Infections  Bacterial / Pyogenic Neurologic Infections  Fever and chills
 Bacterial or Pyogenic Invading organism reach the CNS by:  Nausea & vomiting
- Bacterial meningitis  Vascular system  Back pain
- Brain abscess - systemic  Stiff neck
- Other bacterial infections - blood stream infection  Generalized seizures
 Viral  Direct extension from adjacent cranial  Signs of meningeal irritation
- Viral Meningitis structures - Nuchal rigidity
- Viral Encephalitis - mastoid - (+) Brudzinski’s sign (flexion at the hip &
> Arbovirus encephalitides - nasal sinus fractures knee responsible to forward flexion of neck)
> Herpes simplex virus encephalitis  Iatrogenic - (+) Kernig’s sign (inability to straighten
> Acute anterior poliomyelitis - invasive procedures knee when hip is flexed
 Others  Bacterial Meningitis  Brudzinski’s sign
- Fungal  Involves the arachnoid, subarachnoid space,  Patient in supine, lift the head rapidly up
- Neurosyphilis & pia mater around the brain and spinal cord from the bed
- Disorders due to bacterial toxins  Factors predisposing to bacterial meningitis:  (+) if forward neck flexion produces flexion
> Tetanus - head trauma of both thighs at the hips; and flexure
> Diphtheria - systemic infection movements of the ankles and knees
> Botulism - post-surgical infection  Kernig’s Sign
 Nursing Diagnosis - meningeal infection  Patient in recumbent
 Alteration in comfort: pain due to headache, - anatomic defects  Thigh flexed at right angle to the abdomen
fever, neck pain, meningeal irritation, - other systemic illness  Knee flexed at a 90’ angle to the thigh,
photophobia  Bacterial Meningitis  Then extend the lower leg
 Potential for injury due to restlessness, Pathophysiology  (+) when extending the leg upward causing
disorientation  When pathogenic organisms enter the pain, spasm of the hamstring muscles, &
 Anxiety/fear due to seriousness of condition, subarachnoid space, inflammatory reaction resistance to further leg extension at the
diagnostic & treatment procedures occurs resulting in: knee
 Potential alteration in nutrition, less than - CSF clouding  Bacterial Meningitis
body requirements due to anorexia, nausea, - Exudate formation Diagnosis
fatigue, vomiting - Changes in subarachnoid arteries  assess signs and symptoms
 Nursing Diagnosis - Congestion of adjacent tissues  confirmed by isolating the causative
 Potential alteration in oral mucous  Pia-arachnoid becomes thickened & organism from CSF
membrane due to dehydration, lack of adhesions form  Lumbar puncture
ability for self-care  Bacterial Meningitis  CSF and blood culture
 Knowledge deficit about condition, Etiology - elevated CSF pressures
treatment, prognosis, prevention  Almost any bacteria entering the body can - elevated CSF protein
 Potential infection to others due to infectious cause meningitis - elevated cell count (PMN’s)
nature of organisms  Most common: - decreased CSF glucose
 Alteration in family process due to illness of - Meningococcus (Neisseria meningitidis)  Bacterial Meningitis
a member - Pneumococcus (Streptococcus Management
 Nursing Intervention pneumoniae); very young & >40  Antibiotic
 Administer prescribed antibiotics specific - Haemophilus influenza (children)  Adequate fluid and electrolyte
for the causative organism  Often present in the nasopharynx
  Assess neuro exam frequently to detect early  Occipital lobe  Best control is to identify & eliminate
signs of increasing ICP - visual field abnormalities vectors responsible for transmission
 Anticonvulsants for seizures  Cerebellar  Acute Viral Meningitis
*Bacterial meningitis is a medical emergency and is - posterior headache, nystagmus, ataxia,  “Aseptic” meningitis
fatal within a few days if untreated. signs of increased ICP  Most often due to mumps virus or one of the
 Brain Abscess  Brain stem picornaviruses
 Collection of either encapsulated or free pus - rare and usually found only at autopsy  Subarachnoid space involvement is usually
within brain tissue arising from a primary  Brain Abscess self-limiting (2 weeks)
focus elsewhere (ear, mastoid , nasal Diagnosis  Acute Viral Meningitis
sinuses, lungs)  Assess for neurologic signs and symptoms Signs and Symptoms
 Occasionally due to penetrating head trauma  Confirmed by CT Scan  Drowsiness
or intracranial surgery  Brain Abscess  Photophobia
 Most common causative organisms: Treatment  Headache & pain when moving the eyes
- Streptococci  Surgical drainage  Neck and spine stiffness on flexion
- Staphylococci - excision  Weakness & painful extremities
 Size varies (whole hemisphere or - needle aspiration  (+) Brudzinski’s and Kernig’s sign
microscopic)  Antibiotics  Acute Viral Meningitis
 Brain abscess *Untreated brain abscesses are almost always fatal Diagnosis
Pathophysiology  Other Bacterial Neurologic Infections  Serologic testing
 Early stages, abscess produces  Subdural empyema  Appropriate viral cultures
inflammation, necrotic tissue, & surrounding - suppurative process in cranial subdural Management
edema space  Symptomatic
 Several days, the center of the abscess is  Epidural abscess  Bed rest
purulent, and a wall of granulation tissue - usually associated with cranial bone  Relieve headache, fever & increase comfort
forms, encapsulating the abscess osteomyelitis  Anticonvulsants as prescribed for seizures
 Infection may spread through thin places in  Spinal epidural abscess  Viral Encephalitis
the capsule & other abscesses may develop - abscess under dura in spinal cord  Acute febrile illness
 Brain Abscess  Thrombophlebitis of the large dural sinuses  Signs and Symptoms:
Manifestations - lateral cavernous & superior sagittal - meningeal irritation
 Headache – most common symptom sinuses - seizures
 Clinical indications of infection (fever,  Viral Infections - confusion and delirium
chills)  Usually associated with systemic viral - stupor or coma
 Drowsiness and confusion infections - aphasia
 Transient focal neurologic disorders  Viruses may enter the body via: - motor involvement
 Depressed mental status - respiratory system - involuntary movements
 Brain Abscess - mouth  Arbovirus Encephalitis
Specific Signs and Symptoms - genitalia  Multiply in a blood-sucking vector
 Frontal lobe - insect or animal bite (mosquito or tick)
- headache, drowsiness, impaired mental  Organism invades the CNS via:  Transmitted to humans by the insect’s bite
function, hemiparesis, focal motor seizures, motor - cerebral capillaries  Incidence is seasonal and geographic
dysphasia - choroid plexus  Infection sites are usually microscopic &
 Parietal lobe - along peripheral nerves scattered throughout the cerebral gray &
- focal sensory abnormalities  No adequate treatment white matter
 Temporal lobe  Immunizations are available for few  Herpes Simplex Virus Encephalitis
- headache, changes in behavior and - poliomyelitis  Virus has an affinity for the inferomedial
memory, hearing defects - rabies portions of the frontal and temporal lobes
  Signs and Symptoms:
- similar with other acute encephalitides
- headache, fever, vomiting, seizures, visual
field deficits
- temporal lobe swelling leads to
transtentorial herniation, coma & brain death
 Management
- 10 day IV Adenine arabinoside
(Vidarabine, ara-A)
 Acute Anterior Poliomyelitis
 “Polio”, Infantile paralysis
 Destruction of motor cells (anterior horn
cells in the spinal cord and brain stem –
medulla)
 Flaccid paralysis of muscles innervated by
affected neurons
 Etiology: Poliovirus
 Spreads from the GIT to the nervous system
 Associated paralysis may or may not occur
 Acute Anterior Poliomyelitis
 If paralysis is present, may be spinal or
bulbar
 Spinal paralysis
- restricted to spinal segments
- flaccid
- asymmetrical & scattered in distribution
- tends to be more severe in one extremity
(leg)
- involvement of diaphragm, intercostal
muscles or medulla may produce respiratory
paralysis
- transient bladder paralysis
 Acute Anterior Poliomyelitis
 Bulbar paralysis
- involves the muscles supplied by the
cranial nerves because bulbar nuclei are affected
- these muscles may be paralyzed alone or in
combination with spinal musculature
- often unilateral
- respiratory paralysis results from reticular
formation lesions
 Acute Anterior Poliomyelitis
 Patients with respiratory muscle paralysis
need intensive care
 Mechanical ventilation at the first sign of
respiratory fatigue greatly increases the
chance of recovery
Management
 Mass immunization (infancy) with OPV
 Other Infections
 Fungal
 Neurosyphilis
 Disorders due to bacterial toxins
 Fungal Infections
 May cause
- meningitis
- meningoencephalitis
- intracranial thrombophlebitis
- brain abscess
 Usually a complication from another
condition (leukemia, organ transplant, DM)
that interferes with the body’s normal flora
or suppresses immune response
 Fungal Infections
 Coccidioidomycosis
- mainly involves the lungs occasionally
spreads to the meninges
 Cryptococcosis
- most frequent CNS fungal infection
- Cryptococcus – common soil fungus that
can cause granulomatous meningitis (small
granulomas & cysts within the cortex & large
granulomas & cystic nodules deep within the brain
- Diagnosis: C. neoformans in the CSF
- fatal if untreated
 Fungal Infections
 Mucormycosis
- malignant infection of cerebral vessels
- rare complication of diabetic acidosis
- begins in the nose & paranasal sinuses &
spreads to the brain
 Fungal Infections
 Produce signs and symptoms similar to
bacterial infections
 Main treatment is IV Amphotericin B
 Recovery is almost certain except for
patients with advanced infections or other
overwhelming fatal diseases
 Side effect
- renal toxicity
 Neurosyphilis
 Syphilis affecting the nervous system due to
CNS invasion (within 3-18 months) by
Treponema pallidum
 Does not always develop in patients with
syphilis
 Asymptomatic for the first few years after
infection
 Unless LP is done, the condition remains
undetected at this stage
 Neurosyphilis
 Meningovascular neurosyphilis
- may develop any time after the primary
infection (6 – 7 yrs)
- diffuse or focal
- increased ICP due to hydrocephalus
- indications of cranial nerve damage
- indications of invasion of the brain
parenchyma by granulation tissue
 Neurosyphilis
 Cerebral vascular involvement produces
arterial inflammation leading to fibrosis &
vessel occlusion (CVA)
 Penicillin arrests the disease but neurologic
deficits are irreversible
 Granuloma formation (Gumma) occurs with
focal meningitis
- circumscribed mass of granulation tissue
growing from the pia mater, compressing and
invading brain parenchyma
- does not respond to penicillin
 Neurosyphilis
 Two late forms developing 10 – 20 years
after first infection:
 Tabes dorsalis
- degenerative brain stem changes
- “progressive locomotor ataxia” because
ambulation is affected
- posterior SC columns shrink & fibrosis
develops
- sudden shooting pain in the legs
- ataxia due to sensory deficits
- “slapping” gait
- urinary flow incontinence
- Argyll Robertson pupils
- absent DTRs
 - loss of proprioception - food-borne illness caused by exotoxin
- Charcot joints (painless joint enlargement, Clostridium botulinum which acts at the
hypermobility & deformity) neuromuscular junction causing release of
- Penicillin arrests the condition acetylcholine
 Neurosyphilis - poisoning usually is caused by
 Dementia paralytica inadequately preserved food
- chronic meningoencephalitis which - nausea, vomiting, diarrhea (12-48 hrs after
destroys the cerebral cortex eating contaminated food)
- progressive physical and mental - ocular muscles become involved leading to
deterioration ptosis & paralysis of jaw, trunk & extremities
- Penicillin may arrest the condition but the - sensation & consciousness remain intact
deficits remain - Treatment
- untreated, death occurs in 3 – 4 years > daily antitoxin
 Disorders Due To Bacterial Toxins > ventilatory support
 Tetanus - complete recovery is possible but
- caused by anaerobic spore-forming rod may take months
Clostridium tetani
- spores produce a toxin when introduced to
a wound which suppresses spinal and brain stem
inhibitory neurons and may act directly on skeletal
muscle at the point of entry
- painful muscular spasms & contractions in
the affected extremity
- generalized tetanus (trismus of the jaw
muscles, muscle spasms of neck, trunk, limbs,
respiratory & pharyngeal muscles)
- Treatment:
> DPT immunization (prevention)
> single dose anti-toxin
(hyperimmune serum)
> 10-day course of antibiotic
> isolation in a quiet, dark room
> respiratory support
 Disorders Due To Bacterial Toxins
 Diphtheria
- acute inflammatory disease of the throat
and trachea caused by Corynebacterium diphtheria
which produces toxin that affects the nervous system
- usually begins with paralysis of the palate
& progresses to involvement of cranial nerves V, VI,
X, XII which may become widespread involving
motor & sensory nerves
- no specific treatment
- DPT for prevention
 Disorders Due To Bacterial Toxins
 Botulism

Neurologic Tumors
Stephen Jo T. Bonilla, RN, MD
Department of Surgery
St Luke’s Medical Center
Neurologic Tumors
Central Nervous System Tumors
- Intracranial Tumors
> Primary Intracranial Tumors
> Metastatic Intracranial Tumors
> Granulomas
- Spinal Tumors
Peripheral Nerve Tumors
IntraCranial Pressure (ICP)
Since the skull is a rigid structure housing
the brain, its vasculature(blood), and the
ventricles(CSF), an increase in any of these
constituents or an expanding mass can cause
an increase in ICP
Expanding masses such as a tumor,
hematoma or abscess
Increase in brain water due to edema
Increase in cerebral blood volume due to
arterial vasodilatation or venous outflow
obstruction
Increased CSF due to increased production,
impaired absorption, or flow obstruction
This phenomenon is called hydrocephalus
Effects of Increased ICP
Headache
- Worse in the mornings, aggravated by
bending and stooping
- Become aggravated over weeks to months
- Caused by distortion or irritation of pain
sensitive areas in the dural coverings and blood
vessels
Vomiting
- Caused by compression or ischemia of
brainstem
- Usually occurs with lesions of the posterior
fossa
- Usually the result of hydrocephalus and 4th
ventricle dilation causing stimulation of the nucleus
of vagus nerve
Papilledema
- Usually the result of increased CSF
pressure in the optic nerve sheath impeding venous
drainage and axoplasmic flow in optic neurons
- Swelling of the optic disc and retinal and
disc hemorrhages can occur
- Vision can be compromised when the
condition is severe
Effects of Increased ICP
Personality and behavior changes
- Depression in motor and thought processes
that can lead to somnolence, and decrease of
consciousness and coma
- It is thought that Compression on the
reticular substance of upper brainstem and thalamus
causes this phenomenon
- These symptoms must be distinguished
from deficits due to focal compression of specific
brain areas
The most catastrophic of the clinical effects
are brain shifts or “ cerebral herniations”   - It usually occurs with posterior fossa
These occur because the cranium is divided
by rigid dural folds
- Falx
- Tentorium cerebelli
Therefore, focal expansion of a mass causes
brain tissue to be displaced relative to these
compartments, resulting in herniation
Types of Herniation
Subfalcine
- Unilateral expansion of one cerebral
hemisphere causing the cingulated gyrus to be
displaced under the falx cerebri
- This can cause anterior cerebral artery
compression causing ischemia of the paramedial and
and superior frontal-parietal areas
Types of Herniation
Transtentorial or Uncal herniation
- Displacement of the medial temporal lobe
through the tentorial hiatus
- Tumors of the middle fossa or temporal
lobe
- Ipsilateral 3rd CN becomes compressed
resulting in pupillary dilation (mydriasis) and
oculomotor deficit (ptosis and no pupillary light
reaction)
- Decerebration coma due to midbrain
compression
- Hydrocephalus with obstruction of the
aqueduct of Sylvius, causing even higher ICP
- Contralateral cerebral peduncle becomes
compressed against the free edge of the tentorium
cerebelli. These upper motor neurons have not yet
crossed until they get to the medulla, the result is
ipsilateral motor weakness on the side of the lesion
- Posterior cerebral artery compression and
ischemia of its area of perfusion that can result in
unilateral or bilateral homonymous hemianopia.
Types of Herniation
Tonsillar or cerebellar herniation
- Cerebellar tonsils herniated through the
foramen magnum
- this condition is life-threatening and due to
compression of the brain stem, and vital respiratory
centers in the medulla oblongata
tumors in children
Intracranial Tumors
2nd only to CVA as the most common
endogenous neurologic problem
Skull is rigid and has little room for
expansion
Both benign & malignant tumors are
potentially fatal
- local destruction & brain tissue
compression
- progressively increasing intracranial
pressure causing herniation & death
However, intracranial tumors are not
inevitably fatal.
Outcome depends on the tumor location,
size, and type
Benign tumors may be cured with early
diagnosis & surgery
Occur equally in males & females
Intracranial Tumor According To Age And
Site
Age Cerebral Hemisphere Intrasellar &
Parasellar Posterior Fossa
<20 Ependymomas; Astrocytomas,
Mixed Astrocytomas,
 less commonly gliomas, Inside the brain substance - Headache (localized or generalized),
Ependymomas Medulloblastoma, - gliomas severe in frontal or occipital regions, intermittent &
astrocytomas - hemangiomas increasing in duration
Ependymomas Outside the brain substance - Nausea & vomiting
20-40 Meningiomas, Pituitary - meningeal tumors - Papilledema (edema & hyperemia of the
adenomas; Acoustic neuromas, - cranial nerve tumors optic disc) due to increased pressure in the central
Astrocytomas; less - pituitary tumors retinal vein due to obstructed venous return from the
commonly, Meningiomas, Metastatic Intracranial Tumors eye
less commonly 10-20% of intracranial tumors - Seizures – often the first indication of a
Meningiomas Often the primary sites are tumor
Hemangioblastoma - Lungs (bronchus) - Dizziness & vertigo
metastatic tumors - Breast - Mental status changes
less commonly, Brain tissue reacts severely to the presence Diagnostic Tests For Intracranial Tumors
of metastatic tumors CT Scan
Metastatic tumors Profound swelling and outpouring of Plain skull and chest x-rays (to exclude
>40 Glioblastoma Pituitary phagocytic cells occur metastatic carcinoma)
adenomas; Metastatic tumors, Individual metastatic nodules are usually EEG
multiforme, less well circumscribed Management For Intracranial Tumors
commonly, Acoustic neuromas, As they enlarge, their centers degenerate & Surgery if possible
Metastatic tumors become cystic Radiation therapy
Meningiomas Meningiomas Granulomas Chemotherapy
Intracranial Tumors Tumors or neoplasms composed of - Methotrexate
Surgery is usually the treatment of choice granulation tissue - Nitrosourea
Combination of surgery, radiation & May develop following - Lomustine
chemotherapy - syphilis infections - Semustine
Primary - infection from the larvae of various Reduce increased ICP (Mannitol or urea)
Metastatic intestinal parasites Corticosteroids to reduce cerebral edema
Granulomas - fungal infections Nursing Intervention
Primary Intracranial Tumors - tuberculosis Observe for increasing ICP
Gliomas Assessment Findings For Intracranial Instruct patients to avoid straining
- malignant glial cells arising from various Tumors Observe for early signs of impaired motor
support brain tissues Localized function
- Glioblastoma multiforme (most malignant - destruction, irritation, or compression of Observe for hyperthermia, seizures, pain or
glioma) the part of the brain in or near the tumor vomiting
- Astrocytoma - blood supply to the affected area is Check for significant alterations in vital
- Ependymoma impaired signs
- Medulloblastoma - focal weaknesses (hemiparesis) Assess coping methods of patient and family
- Oligodendroglioma - sensory disturbances (anesthesia) Spinal Tumors
Neuromas or Neurobromas (arise from - language disturbance Similar in nature and origin to intracranial
nerve cells) - coordination disturbances (staggering gait) tumors but occur much less often
Meningiomas (arise from the meninges) - visual disturbances (diplopia, hemianopia) Mostly involves the thoracic region
Hemangiomas (arise from the blood vessels) Assessment Findings For Intracranial Extramedullary (outside the SC)
Development tumors (colloid cysts, dermoid Tumors - Intradural
cysts) General - Extradural
Others (Pineal and Pituitary tumors) - Extravertebral
Primary Intracranial Tumors Intramedullary (inside the SC)
 Most common SC tumors - spastic quadriplegia
- Neurofibromas - sensory changes
- Meningiomas Plain X-rays
Both are benign, operable and may not CT Scan
produce permanent damage if removed early Myelography
Intramedullary Spinal Cord Tumors Management Of SC Tumors
Least commonly occurring SC tumor (10- Surgery
15%) Radiation therapy
Ependymomas & astrocytomas are the most Peripheral Nerve Tumors
common types Solitary tumors (neurofibroma) may develop
Slow, progressive onset on any peripheral nerve
Muscle weakness, localizing pain, atrophy Multiple tumors most often occur and are
& loss of DTRs part of a syndrome known as
Sensory loss for pain and temperature neurofibromatosis (von Recklinghausen’s
Tumors in caudal region result in bowel, disease)
bladder, & sexual dysfunction - Hereditary disorder characterized by
Intradural-Extramedullary SC Tumors multiple tumors of spinal & cranial nerves
Most commonly occurring SC tumor (50%) Usually is not life threatening
Meningiomas & neurofibromas are the most Lesions are excised only when they interfere
common types with normal activity
Thoracic spine is frequent site
Symptoms of cord compression are gradual
or may be incomplete (Brown-sequard
syndrome)
Extradural SC Tumors
Mostly malignant
Rapid onset of symptoms
Local pain at area of tumor on spine & along
spinal nerve dermatomes
Increased pain with bed rest, movement, &
straining
Pain occurs before SC dysfunction
symptoms
Assessment of SC Tumors
Extramedullary Tumors
- early characteristics of SC compression
including pain, sensory loss, muscle weakness, &
wasting
- progressive SC compression is manifested
by spastic weakness below the level of the lesion,
decreased sensation & increased reflexes
- Severe cord compression destroys the cord
& produces paraplegia or quadriplegia
Assessment of SC Tumors
Intramedullary Tumors
- more variable signs and symptoms
  Neurologic Vascular Lesions
 Stephen Jo T. Bonilla, RN, MD
 Department of Surgery
 St. Luke’s Medical Center
 Neurologic Vascular Lesions
 Vascular brain lesions
- Stroke (CVA)
- Transient Ischemic Attack (TIA)
- Intracranial aneurysm and primary
subarachnoid hemorrhage
- Arterio-venous malformation (AVM)
 Vascular spinal cord lesions
- Myelomalacia
- Hematomyelia
 Vascular lesions of the cerebral veins and
sinuses
 Vascular Brain Lesions
 Forms the largest number of neurologic
illnesses
 Significant causes of chronic disability
 Review of the Brain Blood Supply
 Artery
 Vein
 Capillaries
- no fenestrae
- exchanges occur in the cytoplasm
- 2 capillaries arise from 1 arteriole
- no perivascular space
- enclosed by astrocytes
- tight relationship greatly reduces volume
of interstitial in the brain & SC
 Great Arteries
 Cerebral Circulation
 Cerebral Circulation
 Blood is carried to the cerebral hemispheres
& brain stem by two paired systems of
vessels
 Internal carotid artery
- Middle cerebral artery
- Anterior cerebral artery
- Posterior communicating artery
 Vertebral-basilar systems
- Vertebral artery (enters the cranium
through foramen magnum, ascend & join to form the
Basilar artery
 At the base of the brain, the branches of the
internal carotid & vertebral-basilar system
join in a network of vessels called Circle of
Willis
 Cerebral Circulation
 Circle of Willis is a shunting mechanism
between the two systems that allows for a
continual blood supply to the entire brain if
one of these systems is affected by trauma or
other lesions
 Blood drains from the brain by a complex
venous system
 Internal and External veins drain into venous
sinuses in the dura, which ultimately drain
into the internal jugular vein
 Venous System
 Venous Sinuses
 Incorporated in the dura mater
 Falx cerebri – vertical sheet of dura that
separates two cerebral hemispheres
 Corpus callosum – tract that connects the
two cerebral hemispheres
 Tentorium cerebelli – sheet of dura
separating the two cerebral hemispheres
from the cerebellum
 Cerebral Circulation
Brain
 2% of TBW
 20% of cardiac output
 20% of oxygen consumption
 70% of glucose consumption
* If ischemia lasts more than a 10 minutes, cells are
irreversibly damaged & tissue necrosis occurs
 Cerebral Circulation
 Blood supply to the brain may be altered
(slowly or rapidly) by
- Local disorders
> thrombi
> emboli
> hemorrhage
> vascular spasms
- Generalized disorders
> ineffective heart-lung function
 If cerebral circulation is interrupted
extensively, cerebral anoxia develops
 Cerebral Infarction
 Deprivation of blood supply to a localized
area of the brain
 Causes:
- thrombi
- emboli
- blood vessel spasms
 Extent of an infarction depends on factors
such as location & size of the occluded
vessel & adequacy of collateral circulation
to the area supplied by the occluded vessel
 Atherosclerotic disease often affects arteries
leading to the brain but affects vessels
within the brain much less often
 Portions of the circle may also be involved
in thrombosis, clots
 The regional frequency of development of
these blockages and the seriousness of such
strokes depends on the exact location--the
importance of the blocked vessel and the
presence of collateral circulation
 Arteriosclerosis
 Build-up of fatty deposits (cholesterol)
mainly in the tunica media & tunica intima
of middle-sized vessels
 Cerebrovascular Accident
 Most common type of carebrovascular
lesion is a stroke or CVA
 3rd most common cause of death (US)
 Risk Factors
- Previous ischemic episodes
- Cardiac disease: MI, CAD, LVH, CHF
- DM
- HPN
- Hypercholesterolemia
- Smoking
- OCP use
- Emotional stress
- Obesity
- Family history of stroke
- Age
 Cerebrovascular Accident
Etiology
 Thrombosis
- most common cause and is usually due to
atherosclerosis, and rarely due to inflammatory
reactions in vessel walls
 - common site: bifurcation of common
carotid into the internal and external carotid arteries
- tends to develop while a person is asleep or
within hour after arising
- infarcts from thrombosis do not cause
death unless they are massive
 Cerebrovascular Accident
 Thrombosis
> ischemia in the brain tissue supplied by
the affected vessel
> edema and congestion in the surrounding
areas (may cause greater dysfunction)
> edema may subside in a few hours or
several days
> patient may improve & regain some
functions impaired by the edema
 Cerebrovascular Accident
 Cerebral embolism
-occlusion of a cerebral vessel by emboli
(fragments of clotted blood, tumor, fat, bacteria, or
air)
- most often lodges at the bifurcation of the
middle cerebral artery
- necrosis & edema
- if it is septic & infection extends beyond
the walls of the vessel, an abscess forms or
encephalitis develops
- if infection remains contained w/in the
occluded vessel, an aneurysmal dilatation of the
vessels may develop (mycotic aneurysm), and may
rupture
 Cerebrovascular Accident
 Intracerebral hemorrhage
- rupture of a cerebral vessel that causes
bleeding into brain tissue
- usually produce extensive residual function
loss & have the slowest recovery of all types of
stroke
- large hemorrhages usually come from
arteries
- small ones may come from veins &
capillaries
- effects depend on site & extent of the
hemorrhage
- brain herniation causes death in >50% of
patients w/in the first 3 days
- most brain hemorrhages are caused by
rupture of arterioslcerotic & hypertensive vessels
 Cerebrovascular Accident
 Spasm
- due to some irritation of the outer part of
the arterial wall, reduces blood flow to the area of
brain supplied by the constricted vessel
- may not cause permanent brain damage
 Cerebrovascular Accident
 Compression
- may result from tumor, large blood clot,
swollen brain tissue.
 Assessment Findings During Stroke
Progression
 When providing nursing care for people
with strokes, it is important not only to
understand the cause of stroke but also to be
able to recognize its precipitating &
progressive manifestations
 Headache, vomiting, seizures, coma, nuchal
rigidity, fever, hypertension, ECG
abnormalities (prolonged ST segment),
sclerosis of peripheral & retinal vessels,
confusion, disorientation, memory
impairment, & other mental changes
 Assessment Findings During Stroke
Progression
 Focal warning signs:
- hemiplegia, transient loss of speech,
paresthesia involving half of the body
 General warning signs:
- mental confusion, drowsiness, dizziness,
headache
 Complete hemiplegia is common because
the basal ganglia & adjacent internal capsule
are affected >2/3 of the time
 Assessment Findings During Stroke
Progression
 Speech center is usually located in the left
side of the brain producing aphasia & right-
sided hemiplegia
 Extensive cerebral lesions often produce
conjugate deviation of the eyes or head or
both toward the lesion
 Pupillary abnormalities may occur if the
lesion produces edema pressing on the 3rd
cranial nerve in the midbrain
 Assessment Findings During Stroke
Progression
 Thalamic syndrome
- burning or aching dysesthesia involving
half of the body with hands most affected
- pain usually begins several weeks after the
stroke & is intensified by emotional disturbances
 Rarely cause sudden death
 When sudden death does occur, it is usually
due to heart failure
 If an intracerebral hemorrhage ruptures into
the ventricles, ICP increases & outcome is
fatal w/in 3-12 hours
 Assessment Findings During Stroke
Progression
 2 primary causes of death with stroke
- respiratory infection
> impaired consciousness,
attention, feeding & swallowing
> may lead to death from
progressive hypoxia
- brain stem failure
> fever, tachycardia, tachypnea
with deepening coma due to damage to the
vasomotor & heat-regulating centers
 Diagnostic Procedures With Stroke
 CT Scan
- localizes hemorrhages, infarctions, &
subarachnoid clots around aneurysms & ventricular
abnormalities
 Lumbar puncture
- useful if possible SAH is not apparent on
CT scan
 ECG
 Chest x-ray
 CBC, ABG, urinalysis
 Intervention During Acute Phase Of Stroke
First Aid
 Maintain a patent airway
 Loosen tight clothing to facilitate respiration
& circulation to the head
 Send for medical help & keep the person
quiet
  Position an unconscious patient on the side
to facilitate drainage & prevent aspiration
 A conscious patient may be in the most
comfortable position
 Elevate patient’s head to avoid headache
 If patient is cyanotic, administer O2 if
available
 Keep the patient warm
 Offer assurance & explain procedures
 Intervention During Acute Phase Of Stroke
General Care
 Examine head for external injury & presence
of neck stiffness
 Assess neuro VS
 Intervention During Acute Phase Of Stroke
Treatment goals
 Preserve life
 Minimize residual disability
 Prevent recurrence
 Nursing Diagnosis and Intervention
 Potential ineffective airway clearance due to
paralysis, unconsciousness
- insert artificial airway & suction as
necessary
 Alteration in nutrition, less than body
requirements due to unconsciousness,
paralysis
- IVF as ordered
- document I & O
- maintain adequate nutrition
 Nursing Diagnosis and Intervention
 Potential fluid volume deficit
- document I & O
- insert foley catheter
- administer IVF as ordered
 Impaired physical mobility due to
hemiplegia, unconsciousness
- change position frequently
- prevent complications of immobility
(pneumonia, urinary stasis, contractures, pressure
sores)
 Nursing Diagnosis and Intervention
 Alteration in bowel elimination, constipation
due to paralysis
- encourage patient to avoid straining
(increases intracranial & vascular pressures) at bowel
movement
- bowel retraining as soon as possible
 Potential sleep pattern disturbance
- create a restful, quiet atmosphere &
planned periods of rest
- don’t attempt to awake a lethargic patient
 Nursing Diagnosis and Intervention
 Self-care deficit due to paralysis
- protect the eye
- provide mouth care
- focus rehab plans extensively on self-care
deficits & ADL
 Alteration in though process due to
impairment of brain function from stroke
- re-orient the patient as consciousness
returns
 Nursing Intervention
 Assessment
- continuous NVS monitoring
- document changes in the level of
consciousness, motor & sensory functions, aphasia,
respiratory difficulty, visual & perceptual defects
 Administer medications & fluids as
prescribed
- avoid sedatives, tranquilizers & opiates
that depress the respiratory center
 Specific Interventions
 Control of hyperthermia
 Control of seizures
 Treatment of hypertension
 Relief of headache & stiff neck
 Treatment of delirium & restlessness
 Prevention of straining
 Prevention of aspiration, choking, excessive
coughing & vomiting
 Promotion of rest & quiet
 Reduction of increased ICP
 Operative removal of blood clots
 Transient Ischemic Attack (TIA)
 Brief, reversible episodes of neurologic
dysfunction caused by temporary, focal,
cerebral ischemia
 Analogous to angina pectoris
 “intermittent cerebrovascular insufficiency”
 Most common cause: occlusive disease of
the extracranial cerebral vessels
 Most frequent site of occlusion: origin of the
internal carotid artery
 Transient Ischemic Attack
Assessment findings
 Visual, auditory, or vestibular disturbance
 Motor and sensory disturbance
 Headache
 Slowed mental processes
 Seizures
 Transient Ischemic Attack
 Generally lasts for only minutes (2-15 mins)
to an hour
 Often recurrent
 May occur for as long as 2 yrs before
cerebral infarction
 Between episodes, neuro assessment are
usually normal
 TIAs are important warning signs that need
thorough assessment
 Transient Ischemic Attack
Diagnostic Procedures
 Stethoscopic assessment of bruits
 Ophthalmodynamometry (indirect
measurement of pressure in the retinal
artery)
 Angiographic studies of intracranial &
extracranial blood vessels
 Doppler assessment of cerebral blood flow
 Transient Ischemic Attack
Treatment
 Antiplatelet medications
 Surgery
- anastomosis of the superficial temporal
artery to the middle cerebral artery
- endarterectomy
*most successful if done before a stenotic
artery is completely occluded
 Transient Ischemic Attack
Post-op Nursing care
 Keep head in a straight position to help
maintain airway patency & minimize stress
on operative site
 Elevate the head of the bed when VS are
stable
  Assess patient’s breathing pattern, pulse, BP
(120-170 to ensure cerebral perfusion)
 Observe operative site for hematoma,
swelling, abnormal discharge
 Intracranial Aneurysm and Primary
Subarachnoid Hemorrhage
 Most common cause of subarachnoid
bleeding is: meningeal vessel rupture from
head trauma
 Most common cause of spontaneous
subarachnoid hemorrhage is leaking or
rupture of an aneurysm within the
subarachnoid space
 Cause of death in over half of all fatal
cerebrovascular lesions <45 y/o
 Intracranial Aneurysm and Primary
Subarachnoid Hemorrhage
 Aneurysm – localized dilatation or
outpouching of a blood vessel wall
 Rupture is probably due to degenerative
changes in the vessel wall, high blood
pressure, & constant stress caused by the
force of blood flow
Types
 Saccular (berry) aneurysm
- most common & is caused by congenital
weakness in artery walls
- usually have a “neck” or narrowed portion,
attached to the vessel
- most develop around the circle of Willis
 Fusion aneurysm
- most often occur on the large basilar &
carotid arteries
- does not usually rupture
 Intracranial Aneurysm and Primary
Subarachnoid Hemorrhage
Assessment Findings
 Usually asymptomatic until it ruptures
 Mild headache, confusion, fainting, vertigo
 Worst headache (occipital area) with
vomiting, loss of consciousness, lethargic or
comatose within hours
 Generalized seizures, meningeal irritation
due to blood I the subarachnoid space
 Intracranial Aneurysm and Primary
Subarachnoid Hemorrhage
Grading - do not restrain patient as this cause
I minimal bleeding, alert, no agitation & increased ICP
neurologic deficit, no symptoms - restrict visitors according to patient’s
II mild bleeding, alert, headache, wishes or conditions
minimal neurologic deficit (III CN palsy, stiff neck) - elevate head of bed (15 – 30’)
III moderate bleeding, drowsy / - advise patient to avoid straining
confused, headache, stiff neck, with or w/o - place necessary items (call bell) within
neurologic deficit reach
IV moderate to severe bleeding, semi-coma, - assist with position changes & turning
with or w/o neurologic deficit  Intracranial Aneurysm and Primary
V severe bleeding, coma, decerebrate Subarachnoid Hemorrhage
movements, near death Intervention
 Intracranial Aneurysm and Primary  Nursing
Subarachnoid Hemorrhage - Avoid sneezing, coughing, straining,
Diagnosis bending, vomiting & excessive suctioning
 History and PE - enemas are contraindicated
 CT Scan (identify blood in the subarachnoid - do not use rectal thermometers
space, large aneurysms, intracerebral clots - give stool softeners or laxatives as
surrounding an aneurysm) prescribed
 Lumbar puncture (confirms presence of - provide adequate nutrition & hydration as
blood in subarachnoid space prescribed
 Angiography (definitive test) - avoid stimulating foods or beverages
 Intracranial Aneurysm and Primary - administer analgesics or sedatives as
Subarachnoid Hemorrhage prescribed
Complications  Arteriovenous Malformation (AVM)
 Vasospasm  Congenital malformations consisting of
- temporary narrowing of a vessel lumen tangles of thin-walled blood vessels without
- occurs in the vessel adjacent to a ruptured intervening capillaries, thus, local brain
aneurysm & may spread throughout all major vessels tissue perfusion cannot occur
at the base of the brain  Arterial & venous blood shunt together
- produces symptoms of ischemia, infarction  Vessels may leak small amounts of blood or
or permanent neurologic deficit may rupture causing hemorrhage into
- no effective treatment subarachnoid space or brain
 Hydrocephalus  Most commonly occur in the posterior
- blood in the subarachnoid space prevent cerebral hemisphere
adequate CSF circulation  Vascular Spinal Cord Lesions
- often resolves spontaneously or treated by  Blood supply to the spinal cord occurs via
VP shunting the
 Intracranial Aneurysm and Primary - anterior spinal artery (supply most of the
Subarachnoid Hemorrhage cord’s cross sectional area
Intervention - posterior spinal artery (supply the posterior
 Surgical white matter & part of post gray matter)
- aneurysm clipping - radicular arteries (supply the superficial
 Nursing areas of white matter)
- ensure strict bed rest in a quiet
environment
  Complex venous system drains the cord &  Vascular Lesions of Cerebral Veins and
empties into the anterior and posterior spinal Sinuses
veins & two lateral veins  Focal neurologic lesions occur from
 Vascular Spinal Cord Lesions occlusion of the cortical & subcortical veins
 As in the brain, SC vascular lesions may be  Large dural sinuses may become
caused by rupture, thrombosis or embolism thrombosed from infection within or from
 Trauma is the usual cause of hemorrhage the epidural or subdural spaces
into the SC  May be caused by trauma, tumor, or clot
 Embolism of spinal vessels is rare formation in polycythemia
 Arteriosclerosis of spinal vessels is not a  Superior sagittal, lateral & cavernous dural
common cause of thrombosis sinuses are most often thrombosed
 Thrombosis is usually due to meningitis or  Thrombosis of the lateral sinus is usually
compression by tumors, granulomas or due to otitis media & mastoiditis
abscess in the epidural space  Vascular Lesions of Cerebral Veins and
 Vascular Spinal Cord Lesions Sinuses
 Myelomalacia  Cavernous sinus thrombosis
 Hematomyelia - due to suppurative processes in the orbit,
 Myelomalacia nasal sinuses, or upper half of the space
 Softening or infarction of the SC resulting - Patient is acutely ill, febrile with eye pain
from spinal artery occlusion - Visual acuity may or may not be affected
 Serious condition with poor prognosis - Pupils may be small or dilated
 Little or no return to normal function to Treatment
involved areas  Antibiotics
Assessment Findings  Anticoagulants
 Motor paralysis
 Sensory loss below the level of the lesion
with paralysis of bladder & bowel sphincters
 Initially limbs are flaccid with no DTRs;
after several weeks, spasticity &
hyperreflexia develop
Management
 Maintain body function
 Prevent complication of immobility
 Provide pain relief
 Rehab 12 – 14 hrs after onset of symptoms
 Hematomyelia
 Hemorrhage into the substance of the spinal
cord
 Almost always follows trauma but may be
caused by vascular malformation or a
bleeding disorder
 Signs symptoms usually develop suddenly
& depend on the size of hemorrhage
 Immediate surgery to relieve cord
compression is indicated
 Congenital Neurologic Conditions Loss of pain & temp sensation in 1 or both
Stephen Jo T. Bonilla, RN, MD sides of the face
Department of Surgery Nystagmus
St. Luke’s Medical Center Respiratory stridor
Congenital Neurologic Conditions Dysphonia
Acrania Treatment
- absence of the cranium Relieve increased pressure on the cord from
Anencephalus the fluid content of the cavities within the
- absence of the brain spinal canal by removing fluid build-up
Microcephalus Direct surgical drainage
- extremely small brain Shunt placement to restore CSF outflow
Congenital Neurologic Conditions
Hydrocephalus
- excessive enlargement of ventricular
cavities of the brain
Spina bifida
- spinal closure defects
Syringomyelia
Abnormal cavities filled with yellow liquid
in the spinal cord substance, especially the
cervical cord
Scar tissue surrounds the cysts
Characterized by
- muscular weakness & wasting
- various sensory defects
- indications of injury to the SC long tracts
- trophic disturbances
Syringomyelia
Begins at any age (usually 30-40 y/o)
Often occurs with other developmental
defects (kyphosis, scoliosis, clubfoot)
Atrophy, weakness & fibrillations of the
small muscles of the hands
Loss of pain sensation in the fingers or
forearm
Weakness & atrophy of shoulder girdle
muscles
Horner’s syndrome
Nystagmus
Vasomotor disturbances of the upper
extremities
Syringobulbia
Presence of similar cavities in the medulla
oblongata without involving the spinal cord
Atrophy & fibrillation of tongue
  Degenerative Neurologic Conditions
 Stephen Jo T. Bonilla, RN, MD
 Department of Surgery
 St. Luke’s Medical Center
 Degenerative Neurologic Conditions
 Extrapyramidal disorders
- Huntington’s chorea
- Parkinson’s disease
 Amyotrophic lateral sclerosis (ALS; motor
system disease)
 Myasthenia gravis
 Progressive muscular dystrophies
 Alzheimer’s disease
 Extrapyramidal Disorders
- characterized by abnormal involuntary
movements (dyskinesias), spasms, tremors,
disturbances in posture, & muscle tone
changes
- Refers to the components of basal ganglia &
related subcortical nuclei that influence
motor activity responsible for integrating &
coordinating voluntary movement
 Huntington’s chorea
 Parkinson’s disease
 Huntington’s Chorea
 Huntington’s disease / Chronic progressive
chorea
 Hereditary disease of the basal ganglia &
cerebral cortex
 Usually appears in adulthood & is
characterized by
- dominant inheritance (Chromosome 4p)
- choreoathetosis
- progressive dementia
 Huntington’s Chorea
 Degenerative changes in the basal ganglia &
cortical atrophy of the gyri in the frontal &
temporal lobes
 Unknown cause
 Deficiency in GABA (gamma aminobutyric
acid) inhibitory system in the basal ganglia
that leads to excess in the dopaminergic
system leading to typical movements of the
disease
 Huntington’s Chorea
Assessment Findings
 Emotional disturbances and mental
deterioration
- negative, suspicious, & irritable
- gradual loss of self-control, temper
outbursts, severe mood swings, & sexually
promiscuous
- attention span & memory is poor
- may become totally demented, unkempt,
incontinent, & completely helpless
 Huntington’s Chorea
Assessment Findings
 Abnormal movements
- may or may not precede mental &
emotional deterioration
- restless, “fidgety”, rapid & jerky
movements (trunk & limbs)
- facial grimacing & shoulder shrugging
- abnormal movements are aggravated by
stress & emotional situations
 Huntington’s Chorea
Intervention
 No known treatment
 Haloperidol (Haldol)
- dopamine blocker
- may control the abnormal movements &
some behavioral manifestations
 Family with the disorder should receive
genetic counseling
 Parkinson’s Disease
 Paralysis agitans / Parkinson’s syndrome /
Parkinsonism
 Complex clinical syndrome characterized by
disability through loss of motor function
resulting from tremor & rigidity
 Parkinson’s Disease
Forms
 Idiopathic or degenerative (most common)
 Post-encephalitic (rare; sequel to epidemic
encephalitis)
 Atherosclerotic (CNS blood vessel
atherosclerosis can produce some parkinson-
like symptoms)
 Drug-induced (long-term use of haloperidol,
reserpine, phenothiazines)
 Toxic (CO, mercury, manganese)
 Trauma
 Parkinson’s Disease
 Degenerative process involving the basal
ganglia & substantia nigra
 Dopamine is significantly decreased in the
caudate, putamen, & substantia nigra
 Unknown cause
 Develops slowly (50 y/o)
 Cardinal features
- Tremor
- Rigidity
- Akinesia
- Postural instability
 Parkinson’s Disease
Assessment Findings
 Early: slight slowing in the ability to
perform ADL, general feeling of stiffness
 “pill-rolling tremor”; intention tremor
 Akinesia (absence or poverty of movement)
 Dyskinesia (impaired voluntary activity
resulting to incomplete movements)
 Bradykinesia (abnormally slow physical &
mental responses
 Parkinson’s Disease
 Facial expression with advanced disease
appears stiff, masklike, & staring
 Speech is slow, monotonous, low pitched
 Lacrimation, constipation, incontinence,
decreased sexual capacity, excessive
perspiration, heat sensitivity
 Does not usually affect intellectual faculties
 Parkinson’s Disease
Intervention
 No treatment
 L-dopa (L-dihydroxyphenylalanine)
- replenish the neurotransmitters in the
extrapyramidal tracts & provide patient symptomatic
relief
 Levodopa
*Dopamine can not be given because it does not
cross the BBB, however, levodopa (precursor of
dopamine) can cross BBB & converts to dopamine in
the basal ganglia
- CI: narrow-angle glaucoma,
hypersensitivity
- SP: CV & pulmonary disease, asthma,
liver or renal disease
 - avoid Vitamin B6 (reverses the effects) - reading aloud; singing scales; holding a  Motor-System Disease (Motor Neuron
SE: anorexia, N & V, UGIB vowel sound for 5 secs; extend the tongue to the Disease)
 Parkinson’s Disease nose; chin & both sides; diaphragmatic breathing  Primary lateral sclerosis
Intervention  Motor-System Disease (Motor Neuron - spasticity & hyper-reflexia w/ destruction
 Anticholinergic Disease) of upper & lower motor neurons & pyramidal tract
- trihexyphenidyl (Artane); benztropine  Actually several progressive disorders of the fibers
(Cogentin) upper & lower motor neurons in the spinal - spasticity & weakness initially appear in
- used before L-dopa cord, brain stem, & motor cortex the legs, followed after a year or two by upper
- blocks muscarinic receptors at cholinergic characterized by muscular weakness, extremity weakness, twitch & atrophy
synapses within the CNS atrophy, & pyramidal tract signs - least common type
- most effective in relieving tremor &  Amyotrophic lateral sclerosis (ALS) – most - death in 6 yrs
rigidity common form  Werdnig-Holfmann disease
- SE: dry mouth, blurred vision, *incorrectly used to refer to all motor-system - form of the disease affecting infants &
constipation, urinary retention, mental dulling, diseases children
confusion  Motor-System Disease (Motor Neuron  Motor-System Disease (Motor Neuron
- never withdrawn suddenly Disease) Disease)
 Parkinson’s Disease Etiology Intervention
Intervention  Unknown  Only supportive therapy
 Amantadine (Symmetrel)  Enzyme abnormalities  Plan physical activities with energy
- anti-parkinsonism drug with unknown  Metabolic causes conservation & muscle strength in mind
MOA  Stress / trauma  Avoid muscle stress
- well-tolerated but less effective than L-  Autoimmune disease / chronic viral  Prevent respiratory complications
dopa infection  In the latter stage, patient may be totally
 Parkinson’s Disease  Motor-System Disease (Motor Neuron dependent
Nursing Intervention Disease)  Amyotrophic Lateral Sclerosis
 Alteration in bowel elimination, constipation  Degeneration occurs in the motor cells in the  One of the least understood, least treatable
- increase fluid intake & dietary fiber spinal cord, brain stem, & cortex along with and most invariably fatal diseases in
- use stool softeners & mild laxatives secondary degeneration of some motor tracts neurology
- establish a regular time for bowel  Weakness, atrophy, paralysis, & skeletal  The "Iron Horse" played continuously for
movements to develop a habit muscle spasticity the Yankees from 6/1/25 to 4/30/39, 2130
 Impaired mobility due to Parkinson’s  Motor-System Disease (Motor Neuron games, .340 average
disease Disease)  Some studies have found an association
- Physical therapy  Amyotropic lateral sclerosis (ALS) between exceptional athleticism (lifetime
- “gait training” - Lou Gehrig’s disease sweating*, actually) and ALS
- ROM exercises - most common form  Also called Lou Gehrig's Disease, the
 Parkinson’s Disease - hyper-reflexia is combined with neurologist who diagnosed it in the famous
Nursing Intervention amyotrophy baseball player patiently watched the
 Self-care deficit due to disabilities of - disease of middle age, usually 50’s; M>F athlete's back for twenty minutes, noted the
Parkinson’s disease  Progressive spinal muscular atrophy fasciculations which vary so much from
- allow extra time for activities such as - weakness & muscle atrophy w/o evidence muscle to muscle and moment to moment
dressing, bathing & meals of pyramidal tract dysfunction  Gehrig died two years after diagnosis
- give supplementary feedings  Progressive bulbar palsy  Amyotrophic Lateral Sclerosis
 Impaired verbal communication - affects muscle of jaw, face, tongue,  Three football players all on the same 1964
- Exercises using facial muscles to help pharynx, & larynx (muscles innervated by CN 49er's team, subsequently developed ALS
maintain intonation & articulation originating in medulla, midbrain, & pons)  The recent news of Catfish Hunter's
diagnosis underscores the fact that otherwise
 vigorous healthy men, especially athletic
men in their prime, seem to be the most
vulnerable
 The Chronicle article underscores the
yearning to understand the disease and the
association with toxins
 Amyotrophic Lateral Sclerosis
 Fasciculations may be subtle or severe to the
point of "vermiculation" giving a "bag of
worms" appearance, for example, the
infamous "scrotal tongue" when the motor
neurons of the 12th Cranial Nerve in the
brainstem are affected
 ALS is a system disease analogous to
Parkinson's: that is, the neurons affected all
participate in a related function
 In ALS that function is muscle strength
 In Parkinson's, the function is muscle
coordination, initiation and sequencing of
activity and entirely different parts of the
brain are affected in the two diseases
 Amyotrophic Lateral Sclerosis
 Note the sparing of sensory nerve roots and
the atrophy of the motor nerve roots (they
should be of the same or larger thickness)
 A study of recombinant human insulin-like
GROWTH FACTOR I on progression of
ALS on 266 patients concluded that the
growth hormone SLOWED THE DECLINE
OF FUNCTION BY 26% - not a cure but
certainly a contribution to quality of life.
Unfortunately, even a 26% life extension
would only be another 9 months, small
consolation
 Myasthenia Gravis
 Muscular weakness caused by reduction in
available acetylcholine receptors at the
neuromuscular junction
 Autoimmune disease characterized by
fluctuating weakness in certain voluntary
(striated) muscles, especially those
innervated by CN originating in the brain
stem
 Muscles involved are ocular, facial, lingual,
& those of mastication & swallowing
 Affects any age (most common b/w 20 &
30); F>M
 Myasthenia Gravis
 Caused by a defect in the transmission of
nerve impulses at the neuromuscular
junction
Assessment findings
 Onset is insidious & disease progresses
slowly
 Usually no sensory loss, however,
paresthesia & aching of weakened muscles
may occur
 Power of muscle contraction decreases
quickly after few repetitive activities of the
muscles involved
 With rest, the muscles rapidly regain their
strength
 However, some muscles do not recover &
may atrophy mildly
 Myasthenia Gravis
 Ocular muscle involvement is the most
common initial symptom
 Expressionless facial appearance (ptosis,
with tendency for the mouth to hang open);
diplopia, nystagmus
 Death usually is due to respiratory
complications
 Muscles of speech involvement causes nasal
voice
 Aphonia (voice loss)
 Often affects muscles of extremities
(difficulty in brushing, shaving, combing);
bowel & bladder sphincters
 Myasthenia Gravis
Diagnostics
 Dramatic improvement in muscular strength
typically occurs after administration of
neostigmine (Prostigmine) or edrophonium
chloride (Tensilon)
*Have atropine sulfate available to counteract severe
cholinergic reactions (arrhythmia)
 Electrical stimulation demonstrates
fatigability of affected muscles (Jolly
reaction)
 EMG
 Myasthenia Gravis
Intervention
 Medical
- short-acting anticholinesterase
(Neostigmine, Pyridostigmine)
> blocks the breakdown of
acetylcholine at the neuromuscular junction &
inhibit cholinesterase
- Corticosteroids (Prednisone)
> decrease antibody production
 Myasthenia Gravis
 Surgical
- Thymectomy (removal of thymus gland)
- relationship of thymus gland to MG is
unclear
- if done within 2 yrs of onset of the disease,
complete remission occurs in about 40% and 40%
improve considerably
 Myasthenia Gravis
Nursing Intervention
 Alteration in nutrition less than body
requirements
- allow plenty of time for meals
- small, frequent feedings that is easily
swallowed
 Ineffective airway clearance due to dyspnea
& impaired ability to cough and swallow
- encourage deep breathing & coughing
- administer O2 as prescribed
- mechanical ventilation may be necessary
 Myasthenia Gravis
 Impaired physical mobility due to muscular
weakness
- Plan activities to conserve the person’s
energy
- Prevent complications of immobility &
keep patient comfortable
 Progressive Muscular Dystrophies
 Group of progressive, degenerative skeletal
muscle diseases characterized by changes in
muscle fibers rather than in spinal motor
neurons, nerves, or nerve endings
 Pathologic changes are confined to the
muscles and do not involve the peripheral &
CNS
 Symmetric muscular weakness & atrophy
with intact sensation
  Muscles of the girdle, proximal limbs, &
eyes are primarily affected
 Progressive Muscular Dystrophies
 Unknown cause
Classification
 Duchenne’s type / Severe generalized
muscular dystrophy of childhood
- begins early in childhood & progresses
rapidly to death by age 20
 Facioscapulohumeral dystrophy
- milder, slowly progressive muscular
dystrophy confined to facial & shoulder muscles
initially
- onset occurs in adolescence
- scapula become winged & upper arms
thinner than the forearms (“Popeye” effect)
 No specific treatment
 Alzheimer’s Disease
 Most common, irreversible dementia
 Dementias are a broad diagnostic category
in which the main assessment finding is
deterioration in intellectual functioning due
to pathologic changes
 Not part of aging process
 Dementias can be caused by more than 50
diseases, however, more than half of all
people who have dementias have
Alzheimer’s disease
 Alzheimer’s Disease
 Severe disorder of cognition and widespread
brain atrophy, gradual, progressive and fatal
 Death usually occurs 2 – 4 years after
diagnosis
 Unknown cause
 Reduced neurotransmitters (somatostatin &
choline acetyltransferase) in the
hippocampus & cortex which accounts for
memory loss
 Predisposing factors
- genetic
- unknown environmental factors
 Alzheimer’s Disease
 Enlarged ventricles
 Loss of brain weight
 Loss of neurons in the basal ganglia,
substantia nigra, & cortex (neurons
responsible for higher cerebral functions - encourage patient to do as much as
such as memory, cognition & thought) possible independently & to dress attractively
 Patients may look well but have difficulty - assist as necessary to prevent frustration
concentrating at all times, short-term - anticipate hygiene needs
memory problems, inappropriate behavior
 Depressed, withdrawn, a little forgetful
 Abstract thinking & decision making
becomes difficult
 Alzheimer’s Disease
 Problems of memory, reasoning, judgment,
& social interaction become pronounced
 Balance is unsteady & stooped posture
develops
 Swallowing may become difficult
 Severe memory loss causes the person to
become lost & forget to eat, drink, etc
 Wakefulness at night is common
 Patient may be incontinent of feces and
urine
 Alzheimer’s Disease
Nursing Intervention
 Alteration in thought processes due to
neuronal degeneration
- address a patient by name
- approach the person in a quiet, calm, &
kind manner
- face the patient when speaking & speak
slowly, use simple sentences
- give clear, simple directions, one at a time
- listen carefully & focus on the patient’s
appropriate behavior
- help patient with telephone numbers
- re-orient the person as necessary
- place calendar & clock in obvious places
- allow patient to reminisce
 Alzheimer’s Disease
 Potential for injury due to impaired
judgment & forgetfulness
- assist with adequate clothing & bedding
for warmth
- pneumonia is a major cause of death
- minimize environmental hazards
 Self-care deficit due to inability to perform
activities of daily living, forgetfulness,
frustration
 Neurologic Demyelinating Disorders - diplopia, dizziness, nystagmus, nausea &
 Stephen Jo T. Bonilla, RN, MD vomiting, signs of facial trigeminal nerve
 Department of Surgery involvement
 St. Luke’s Medical Center  Indications of bladder dysfunction
 Demyelination  Dull, low-back pain or burning leg pains
 Myelin breakdown  Apathy, euphoria, inattentiveness
 Occurs secondarily to infection, deficiency  Multiple Sclerosis
states, intoxication, or neurologic  Charcot’s triad
degeneration - nystagmus
 Acute disseminated encephalomyelitis - intention tremor
 Diffuse cerebral sclerosis - slow enunciation with scanning speech
 Necrotizing hemorrhagic encephalopathy (tendency to hesitate at the beginning of a word or
 Multiple sclerosis – most common syllable)
demyelinating disorders  Multiple Sclerosis
 Unknown cause  No cure
 Viral infections and genetic may contribute  Intervention is symptomatic
 Multiple Sclerosis  Promote rest & avoid stressful situations
 Chronic disabling illness affecting young  Keep the body cool w/ cool baths or ice
adults packs
 Multifocal areas of demyelination diffusely  Regular passive ROM exercises to prevent
scattered throughout the CNS contractures if the person is restricted to bed
 Periods of symptom remission &  Help person & significant others cope with
exacerbation w/ overall progressive decline stress
 Incidence among women almost twice
among men
 20 – 40 yrs
 Cool, temperate climate
 Multiple Sclerosis
 Because the lesions of MS are diffusely
scattered throughout the brain & spinal cord,
the signs & symptoms of MS are highly
individualized
 Weakness and paresthesia in 1 or more
limbs
 Extremity motor weakness (legs) usually the
first symptom
 Lhermitte’s sign –”electric sensation” down
the back following passive flexion of neck
 Retrobulbar (optic) neuritis producing
partial or total loss of vision in one eye
 Multiple Sclerosis
 Unsteady gait, cerebellar ataxia (broad-
based, uncoordinated gait)
 Brain stem involvement
  Neurologic Paroxysmal Disorders  Classification of Seizures  “Little” or minor seizures usually begin
 Stephen Jo T. Bonilla, RN, MD  Generalized during childhood & consists of brief periods
 Department of Surgery - Tonic-clonic (grand mal) of altered consciousness ( 5 – 30 secs)
 St. Luke’s Medical Center - Absence (petit mal)  Diminish after puberty
 Neurologic Paroxysmal Disorders - Minor motor seizures (akinetic, myoclonic,  Grand mal seizures may develop
 Epilepsy atonic)  Unknown cause, birth injuries, acute febrile
- Generalized seizures  Partial (Focal) childhood infections
> Grand mal - Partial seizures with motor components  Minor Motor Seizures
> Petit mal - Partial seizures with sensory components  Myoclonic
> Minor motor - Partial seizures with complex - involuntary jerking contractions of major
- Partial symptomatology muscles
> Partial motor - Partial seizures that secondarily generalize  Akinetic
> Partial sensory  Grand Mal (Tonic-clonic) Seizures - momentary loss of muscle movement
> Partial seizures w/ complex  Sudden loss of consciousness  Atonic
symptomatology  Tonic phase (30 – 60 seconds) - total loss of muscle tone & person falls to
- Status Epilepticus - entire body stiffens in rigid tonic the floor
 Meniere’s disease contraction  Partial (Focal) Seizures
 Headache - patient standing or sitting may fall with  Most common type of epilepsy
- Migraine epileptic cry  Partial motor seizures
- Cluster - respirations are interrupted temporarily &  Partial sensory seizures
- Tension (muscle contraction headache) patient becomes cyanotic  Partial seizures with complex
- Head pain related to eyes, ears, teeth, - jaws are fixed & hands clenched symptomatology
paranasal sinuses - eyes may be opened widely; pupils are  Partial Motor Seizures
 Epilepsy fixed & dilated  Arise from a focus in the region of the
 Seizure disorder  Clonic phase brain’s motor cortex (posterior frontal lobe)
 Epilepsia – take hold of - rhythmic, jerky contraction & relaxation of  Most focal motor seizures begin in the hand
 Viewed as divine origin (“sacred disease”) all body muscles (extremities) & fingers & spread centrally & involve the
 Paroxysmal neurologic disorders causing - urinary & fecal incontinence entire limb – Jacksonian march
recurrent episodes of - may bite the lips, tongue, & inside of  May generalize into grand mal seizure
- loss of consciousness mouth  Partial Sensory Seizures
- convulsive movements - respirations are jerky & stertorous  Transient
- sensory phenomena - excessive saliva causing froth at the lips  Parietal – numbness and tingling
- behavioral abnormalities  Grand Mal (Tonic-clonic) Seizures  Occipital – bright, flashing lights in the field
 Definition of Terms  May last from 2 – 5 mins of vision
 Seizure – paroxysmal, uncontrolled,  Person then relaxes & remains totally  Partial Seizures with Complex
abnormal discharge of electrical activity in unresponsive for a time Symptomatology
the brain’s gray matter  May rouse briefly & then go to a post-ictal  Usually arise from the anterior temporal
 Prodromal phase – precedes some seizures sleep (30 mins – hours) followed by fatigue, lobe
(mins to hours); depression or anxiety depression, confusion, or headache  “Psychomotor or partial complex seizures”
 Aura – brief sensory experience (weakness,  Complete amnesia for the seizure episode &  Frequently begin with an aura; “Déjà vu” is
dizziness, numbness, odor) that occurs at the may feel nauseated, stiff & sore common
onset of some seizures  Examine patient for bruises, lacerations, or  Automatisms during seizures (purposeless,
 Epileptic cry – caused by thoracic & fractures repetitive activities – lip smacking, chewing,
abdominal spasms which expels air through  Petit Mal (Absence) Seizures picking at clothes) while the patient is in a
the narrowed spastic glottis dreamy state
 Ictus – synonymous with seizure
  Partial Seizures that Secondarily  Physical and Neurological Examination  Degeneration of tiny cochlear hair cells
Generalized  Skull x-rays  Meniere’s Disease
 Starts from a particular focus & then the  EEG  Severe rotational type of vertigo
electrical discharges spread throughout the - helps locate the focus of abnormal accompanied by nausea & vomiting,
brain electrical discharges diaphoresis, tinnitus, hearing loss & feeling
 Status Epilepticus - establish a diagnosis of epilepsy of pressure in ear
 State in which a person has continuous - identify specific types of seizures  Nystagmus, brief loss of consciousness
seizures or seizures in rapid succession  CT Scan  Unilateral in most patients
lasting at least 30 mins  Seizures  Diagnosis depends on history, audiometric
 May remain comatose & have repetitive  Eliminate causative factors tests, caloric test
seizures for hours which is exhausting &  Medical  Meniere’s Disease
dangerous - Primary anticonvulsants Acute
 May be precipitated by sudden withdrawal > provide complete seizure control  Bed rest is the most effective treatment
of anti-convulsant medications > Phenytoin  Diazepam slow IV
 Medical emergency > Carbamazepine  Advise patient not to read & avoid bright
 Status Epilepticus > Phenobarbital light
 Maintain a clear airway > Valproic acid  Symptoms should subside in an hour or so
 Prevent aspiration & provide adequate Long-term
oxygenation  Seizures  Medications
 Assess patient constantly - Secondary anticonvulsants - antihistamine, diuretics
 Protect the patient from injury > rarely provide seizure control  Emotional support
 Administer prescribed emergency anti- alone, but produce significant improvements  Dietary management
convulsant in control when given w/ a primary  Identify factors the precipitate episodes
- Diazepam (Valium) anticonvulsant  Meniere’s Disease
- Phenytoin (Dilantin) > Succinimides (Phensuximide,  If patient does not respond to medications,
 Seizures Methsuximide) surgery may be necessary
Etiology > BDZ (Diazepam, Clonazepam)  Shunting or decompression of the
 Symptomatic or secondary epilepsy - Ancillary drugs endolymphatic sac & part of vestibular
- assessment can determine the probable > enhance the effect of an nerve via the middle fossa
cause established anticonvulsant program  Meniere’s Disease
 Idiopathic or primary > Acetazolamide (Diamox) Nursing Intervention
- assessment can not determine the probable  Seizures  Provide understanding & emotional support
cause Nursing intervention  Provide learning/teaching opportunities
 Seizures  Not usually treated by hospitalization  Provide a quiet, safe environment during
 Hyperpyrexia  Support & educate patients with epilepsy & acute episodes
 CNS infections their significant others  Administer medications as prescribed
 Cerebral hypoxia  Help patient identify factors that precipitate  Headache
 Toxic agents seizures  Most common of pains, may occur in the
 Cerebral trauma - stress, lack of sleep, emotional upset, absence of organic disease or as a
 Electric stimulation alcohol use manifestation of serious disease
 Expanding brain lesions  Meniere’s Disease  Most are transient, however, few are intense,
 Anaphylaxis  Chronic disorder of the inner ear, chronic, recurrent
 Degenerative brain disorders characterized by recurring episodes of  Most self-treat with OTC drugs
 Seizures vertigo, associated with tinnitus, & deafness  Encourage patients with persistent or
 History  40 – 50 yrs old recurrent headaches to seek neurologic
 Mental Status Examination  Unknown cause assessment
Types  Histamine headache
 Migraine  Most do not have a history of migraine
 Cluster headaches headaches
 Tension headaches  Excruciatingly painful, unilateral & tend to
 Head pain related to the eyes, ears, teeth, & occur in clusters
paranasal structures  Usually no aura
 Migraine Headache  Episodes usually begin in middle life (M>F)
 Recurrent throbbing headaches at irregular & is worsened by alcohol consumption
intervals  Unknown cause
 Begin during puberty (20 – 40) & decrease  Histamine sensitivity?
in frequency & severity with advancing  Intervention is ineffective because of the
years shortness of episodes
 5-10%; F > M  Tension Headaches
 Pathophysiology is complex  Muscle contraction headaches
 Vascular theory  Result from long-sustained contraction of
 Psychosocial factors skeletal muscles around the scalp, face,
 Precipitated by repetitive conditions neck, & upper back
(fatigue, hunger, refractive errors, bright  Muscles become tender & is associated with
light, surprises, mental & emotional excessive emotional tension, anxiety &
excitement, excessive smoking, alcohol depression
 Classic or Typical Migraine  Begin in adolescence
 May be preceded by an aura or prodromal  Premenstrual
phase  Treatment is symptomatic
 Transient neurologic disturbances (flashes of  Head Pain Related to the Eyes, Ears, Teeth,
light, distorted vision, diplopia, vertigo) & Paranasals
 “Crescendo” quality  Eyes
 Dull, boring, pressing, throbbing or - errors of refraction, glaucoma,
hammering headache, usually unilateral & inflammation, ocular muscle disturbances
may be localized to the front, back or side of  Ears
the head (temple or eyes) - primary ear disorders, inflammatory,
 Patient may be irritable, with nausea & destructive
vomiting, diarrhea (“sick headaches”)  Teeth
 Atypical or Common Migraine - toothache from prolonged muscle
 Begins suddenly with or without prodromal contraction
symptoms, generalized or unilateral & may  Paranasal structures
or may not be accompanied with nausea & - sinusitis
vomiting
 Migraine
 Prevent episodes
 Analgesics for mild to moderate headaches
 Ergot for severe headaches
 Apply pressure on the common carotid
artery
 Dark, quiet room with damp compresses on
the head
 Cluster Headache
  Cranial And Peripheral Nerve Disorders
 Stephen Jo T. Bonilla, RN, MD
 Department of Surgery
 St. Luke’s Medical Center
 Cranial and Peripheral Nerve Disorders
 Cranial Nerves
- Fifth cranial nerve (Trigeminal neuralgia)
- Seventh cranial nerve (Facial paralysis;
Bell’s palsy)
- Eight cranial nerve disorders
 Polyneuropathies
- Guillain-Barre syndrome
 Fifth (Trigeminal) Cranial Nerve
 Trigeminal neuralgia
- most agonizing benign condition & has
been known to prompt severe depression & suicide
 Tic douloureux (repeated wincing in
response to severe pain)
 Unknown etiology
 3 divisions
- ophthalmic
- maxillary
- mandibular
 Trigeminal Neuralgia
 Sudden, excruciating, recurrent paroxysms
of sharp, stabbing pains in the sensory
distribution of 1 or more of 5th CN’s 3
branches
 Maxillary & mandibular branches are most
commonly affected
 Episodes are characterized by the presence
of sensitive trigger zones, which set off a
paroxysm of pain when stimulated
 Trigeminal Neuralgia
 Trigger zones are often small areas on a
person’s upper & lower lips, gums, side of
nose or cheek
 A fearful patient may prevent paroxysms of
pain by
- going w/o nourishment, oral hygiene, or
shaving for days
- trying to keep the face immobile while
talking
- keeping the face & head covered
 Pain may interfere with sleep
 Trigeminal Neuralgia
 Most frequent of all primary neuralgias
 F>M in middle or late life
 Etiology (trauma, infection, vascular
compression, neoplasm, & multiple
sclerosis)
 Trigeminal Neuralgia
Intervention
 No safe, proven, totally successful
 Baclofen (Lioresal) provides relief for some
people with trigeminal neuralgia
 Phenytoin (Dilantin) prevents recurrent
episodes
 Carbamazepine (Tegretol) provide relief for
months to years
SE: thrombocytopenia, leukopenia,
agranulocytosis, and aplastic anemia
 Trigeminal Neuralgia
 Alteration in comfort: pain due to trigeminal
neuralgia
- assess & document neuralgia pain episode,
including precipitating factors, trigger zone locations,
pain description, & ways by which the patient tries to
prevent the pain
- hot or cold foods & fluids may trigger or
increase pain
- protect the patient from jarring movements
- administer medications as prescribed
 Seventh (Facial) Cranial Nerve
 Bell’s palsy
- most common type of peripheral facial
paralysis
- unilateral paralysis of the facial muscles of
expression with no evidence of a pathologic cause
- upward movement of the eyeball on
closing the eye (Bell’s phenomenon)
- drooping of the mouth
- flattening of the nasolabial fold
- widening of palpebral fissure
- slight lag in closing the eye
- eating may be difficult
 Seventh (Facial) Cranial Nerve
 Bell’s palsy
- no known cure
- analgesics
- cortisone (to decrease nerve swelling)
- physiotherapy, moist heat, gentle massage
- corneal protection with artificial tear
solution, glasses, eye patch at night
- patients may think the have had a stroke,
so reassure patients that this is not true
 Eight (Acoustic) Cranial Nerve
 Loss of hearing & tinnitus with involvement
of the auditory branch
 Vertigo, equilibrium disturbance, &
impaired ocular movements with
involvement of the vestibular portion
 No specific intervention
 Polyneuropathies
 Polyneuritis (multiple peripheral neuritis) is
a clinical syndrome produced by widespread
peripheral nerve involvement, causing
sensory loss & impaired reflexes
 Often relates to either a toxic or metabolic
condition
 Gullain-Barre Syndrome
 Inflammatory disease of unknown etiology
involving demyelination & degeneration of
myelin sheath, cylinders of peripheral
nerves, & anterior and posterior spinal cord
roots at spinal segment levels
 Most rapidly developing & potentially fatal
polyneuropathy
 Gullain-Barre Syndrome
 Unknown cause but may be due to an
autoimmune reaction directed at peripheral
nerves
 Inflammatory cells (lymphocytes) enter the
perivascular spaces, causing demyelination
& nerve degeneration
 Usually preceded by a viral infection or by
surgery
 Gullain-Barre Syndrome
 Initial symptoms (paresthesia, pain &
stiffness in the limbs followed by
generalized limb weakness with or without
CN deficits)
 Weakness begins in the legs & ascends to
the trunk, arms & scalp muscle
 Total motor paralysis may occur within a
few days (10-14 days)
 7th CN is most frequently affected
 Gullain-Barre Syndrome
 Mechanical ventilation may be required
 Control infection & prevent complications
of immobility
 Maintain proper body alignment to prevent
deformities
 Nursing Care of Neurosurgery Patients
 Stephen Jo T. Bonilla, RN, MD
 Department of Surgery
St. Luke’s Medical Center
 Nursing and Neurosurgery
 Nursing actions can influence the success or
failure of neurosurgical intervention
 Improved clinical care of unconscious &
head-injured people makes neurosurgery
more effective
 Nurses are especially effective in keeping
foremost the needs of individuals
experiencing neurosurgery, ensuring that the
technology of neurosurgery does not
overwhelm the human beings involved
 Nursing and Neurosurgery
 Neurosurgery encompasses surgery on the
- brain & related structures
- spinal cord & related structures
- peripheral nerves
 Extracerebral neurosurgery (burr holing)
 Extracranial neurosurgery (vascular, spinal,
peripheral structures)
 Intracranial neurosurgery (craniotomy to
remove a brain tumor)
 Spinal neurosurgery (relieve SC
compression or repair herniated
intervertebral disks)
 Peripheral nerve neurosurgery (hand
surgery)
 Intracranial Surgery
 Craniotomy – surgical opening into the skull
- osteoplastic bone flap
- free form flap
- enlarging burr hole
 Craniectomy – a portion of cranium is
permanently removed
 Pre-op Care for Intracranial Surgery
 Psychosocial preparation
 Potential complications may be fatal
 Legal preparation
 Scalp preparation
 Baseline pre-op data
 Post-op Care for Intracranial Surgery
 Potential ineffective airway clearance due to
brain damage and/or prolonged immobility
during surgery
- assess respiratory parameters frequently to
avoid hypercapnia
- maintain airway patency
- do not suction through the nose
- monitor ABG
 Post-op Care for Intracranial Surgery
 Potential sensory-perceptual alteration
and/or impaired physical mobility due to
raised ICP and/or surgical tissue removal or
trauma
- compare pre-op and post-op assessment
findings
- protect patient from harm & seizures
- monitor I & O accurately
 Post-op Care for Intracranial Surgery
 Potential tissue perfusion alteration due to
raised ICP, immobility, and/or surgical
tissue trauma
- correct post-op positioning is extremely
important to prevent pressure on brain’s operative
site, prevent or minimize ICP increase, facilitate
circulation & prevent pressure sores
 Post-op Care for Intracranial Surgery
 Potential impairment of skin integrity due to
surgical incision
- frequently assess condition of head
dressing
- inspect for bleeding or CSF leak
 Post-op Care for Intracranial Surgery
 Impaired physical mobility due to post-op
status and requirements
- frequent position changes very carefully
- do not make the patient strain
 Post-op Care for Intracranial Surgery
 Self-care deficit
- assist in bathing, hygiene, feeding,
toileting, dressing or grooming
 Alteration in comfort due to pain
- keep the environment quiet, calm, & dimly
lit
- Administer prescribed medications