Assessing Client with Neurologic Dysfunction

Health History

- Neurologic Diseases may be

o Stable or progressive
o Intermittent symptom-free periods, with flunctuations
- Health History includes:
o Timing (onset, duration, frequency), Character, Severity, Location
o Precipitating, Aggravating, and Relieving factors
o Progression, Remission, Exacerbation
o Presence or absence of similar symptoms in family members (Family History)

Nervous System Review

- Neurologic Examination
o Mental Status Exam
o Cranial Nerve Testing
o Cerebellar Function
o Sensory Function
o Motor Function
o Reflexes
- Neuro Check
o Level of consciousness
o Glasgow Coma Scale
o Full Outline Unresponsiveness
o Pupillary Reaction and Eye movement
o Respiratory Pattern

Mental Status Exam

- General appearance and behaviors

- Intellectual function
o Memory (recent, remote), attention span, cognitive skills
- Emotional status
- Thought content
- Language/Speech
o Expressive Aphasia: inability to speak
o Receptive Aphasia: inability to understand spoken words
o Dysarthria: Difficulty speech due to impairment of muscles involved in the
production of speech.
- Level of consciousness
o Single most sensitive indicator of changes in neurological status
o Orientation 3x
o Speech: clear, garbled, rambling
o Ability to follow commands
 Level 1: Conscious, Coherent, Cognitive
 Level 2: Confused, Drowsy, Lethargic, Somnolent, Obtunded
 Level 3: stuporous
 Level 4: Coma (light or deep)

The Glasgow Coma Scale

- Eye opening
o 4- spontaneous
 o 3- Verbal
o 2- pain
o 1- no eye opening
- Best verbal response
o 5- oriented 3x
o 4- conversational, confused
o 3- comprehensible words
o 2- incomprehensible, groans
o 1- no response
- Best motor response
o 6- obeys commands
o 5- localizes, painful stimuli
o 4- flexion withdrawal
o 3- decorticate (ab flexion)
o 2- decerebrate (ab extension)
o 1- no motor responses

Full Outline Unresponsiveness (FOUR)

- Eye Response
o Grade the best Response after atleast 3 trials in an attempt to elicit the best level
of alertness. A score of E4 indicates at least 3 voluntary excursions. If eyes are
closed, the examiner should open them and examine tracking of finger or object.
Tracking with the opening of 1 eyelid will suffice in cases of eyelid edema or
facial trauma. If tracking is absent horizontally, examine vertical tracking.
Alternately, 2 blinks on command should be documented. This will recognize a
locked-in syndrome (patient is fully aware). A score of E3 indicates the absence of
voluntary tracking with open eyes. A score of E2 indicates eyelids opening to loud
voices. A score of E1 indicates eyelids open to pain stimulus. A score of E0
indicates no eyelids opening to pain
 4- eyelids open or opened, tracking or blinking to command
 3- eyelids open but not tracking
 2- eyelids closed but open to loud voice
 1- eyelids closed but open to pain
 0- eyelids remain closed with pain
- Motor response
o Grade the test possible response of the arms. A score of M4 indicates that the
patient demonstrated at least 1 of 3 hand positions (thumbs up, fist or peace sign)
with either hand. A score of M3 indicates that the patients touched the examiner’s
hand after a painful stimulus compressing the temporomandibular joint or
supraorbital nerve (localization). A score of M2 indicates any flexion movement
of the upper limbs. A score of M1 indicates exterior posturing. A score of M0
indicates no motor response or myoclonus status epilepticus
o Motor response
 4- Thumbs up, fist or peace sign to command
 3- localizing to pain
 2- flexion response to pain
 1- extensor posturing
 0- no response to pain or generalized myoclonus status epilepticus
- Brain stem reflexes
o Grade the best responses. Examine pupillary and corneal reflexes. Perferably,
corneal reflexes are tested by instilling 2-3 drops of sterile saline on the cornea
from a distance of 4-6 inches (this minimizes corneal trauma from repeated
examinations). Cotton swabs can also be used. The cough reflex to tracheal
suctioning is tested only when both of these reflexes are absent. A score of B4
 indicates pupil and cornea reflexes are present. A score of B3 indicated one pupil
wide and fixed. A score of B2 indicates either pupil or cornea reflexes are absent.
A score of B1 indicates both pupil and cornea reflexes are absent and a score of
B0 indicates pupil, cornea and cough reflexes (using tracheal suctioning) are
absent
o Brain stem reflexes
 4- Pupil and corneal reflexes present
 3- One pupil wide and fixed
 2- pupil or corneal reflexes absent
 1- pupil and corneal reflexes absent
 0- Absent pupil, corneal and cough reflexes
- Respiration
o Determine spontaneous breathing pattern in a nonintubated patient and grade
simple as regular R4, Irregular R2 or Cheyne-Stoke R3 breathing. In
mechanically ventilated patients, assess the pressure waveform of spontaneous
respiratory pattern or the patient triggering of the ventilator R1. The ventilator
monitor displaying respiratory patterns in used to identify the patient-generated
breaths on the ventilator. No adjustments are made to the ventilator while the
patient is graded, but grading is done preferably with PaCO2 within normal limits.
A standard apnea (oxygen-diffusion test may be needed when patient breathes at
ventilator rate R0
 4- not intubated, regular breathing pattern
 3- not intubated, Cheyne-stokes breathing pattern
 2- not intubated, irregular breathing pattern
 1- breathes above ventilator rate
 0- breathes at ventilator rate or apnea

Motor function and Sensory Function

- Motor Function
o Muscle Size
o Tone
o Strength
o Abnormal or Involuntary Movement
- Sensory Function
o Light Touch
o Superficial Pain
o Temperature

Functions of the Nervous System

- Sensory function
o Detects internal and external stimuli
o Carried into the spinal cord and brain
- Integrative function
o Processes sensory information by analyzing sand storing some of it and by
making decisions for appropriate responses
- Motor function
o Elicit appropriate motor responses by activating effectors
o General appearance
 Involuntary, uncoordinated movements
 Facial symmetry
o Muscular power (quadri, para, hemi)
 Weakness (paresis)
 Paralysis (plegia)
o Agnosia: inability to perceive stimuli
o Apraxia: inability to perform fine motor activity
 o Agraphia: inability to write

Pupillary Reaction and Eye Movement

- Observe for pupil’s size, shape and equality of pupils

- Reaction to light: pupillary constriction
- Corneal reflex: blinking reflex in response to light stroking of the cornea
- Oculocephalic Reflex (Doll’s Eyes): Present in unconscious patient with intact brainstem

Respiratory Patterns

- Cheyne-Stroke breathing
o Regular, rhythmic alternating between hyperventilation and apnea
o May be caused by structural cerebral dysfunction or by metabolic problems
- Central neurogenic hyperventilation
o Sustained, rapid, regular respiration
o RR: 25cpm, Normal O2 level
o May be due to brain stem dysfunction
- Apneustic breathing
o Prolonged inspiratory phase, followed by 2-3 second pause
o Usually indicates dysfunction in the pons
- Cluster breathing
o Clusters of irregular breathing, followed by periods of apnea
o Usually caused by lesions of the upper medulla and lower pons
- Ataxic breathing
o Breathing pattern completely irregular
o May indicate damage to respiratory centers of the medulla

Symptomatology

- Pain
- Seizure
- Dizziness
- Visual Disturbances
- Weakness
- Abnormal Sensation
- Incoordination
- Coma
- Delirium and dementia
- Memory impairment
- Tremors

Pain

- Unpleasant sensory perception and emotional experience associated with actual or

potential tissue damage
- Entire subjective
o P- Precipitating/Provocative Factors
o Q- Quality (Character)
o R- Relieving Factors
o S- Severity
o T- Timing (Onset, Duration, Frequency)

Seizure

- Results of abnormal paroxysmal discharges in the cerebral cortex, which then manifest as
an alternation in sensation, behavior, movement, perception and consciousness
- May be the first observable sign of a brain lesion
Dizziness

- Abnormal sensation of imbalance or movement

- Common: elderly
- Difficulty in assessing
o Vague and varied terms used to describe the sensation
- Vertigo
o Specific form of vertigo
o Usually a manifestation of vestibular dysfunction
o May result to spatial disorientation, loss of equilibrium and nausea and vomiting

Muscle Weakness

- Frequently coexists with other symptoms of disease

- Can affect a variety of muscles, causing a wide range of disability
- May be sudden, permanent, or progressive
- Muscles strength testing
o Assessing patient’s ability to flex or extend the extremities against resistance
o Compare the sides of the body to each other
o Done by placing the muscle at disadvantage

Muscle Weakness

5 Normal Muscle strength

- Full power of contraction against
gravity and resistance
4 Slight Weakness
- Fair, but not full strength and
moderate amount of resistance
3 Moderate Weakness
- Just sufficient strength to overcome
gravity
2 Severe Weakness
- Ability to move but cannot
overcome the force of gravity
1 Very severe Weakness
- Minimal contractile power
- Visible or palpable contraction but
no movement noticeable
0 Complete paralysis
- Elicits no response

Ataxia

- Gross of lack of coordination in muscle movement

- Inability of the cerebellum to coordinate movement
- Can be also produced by dysfunction to other regions of the brain
- Assess
o Age
o Acuity
o Circumstances of onset
o Associated findings
- Further Assessment
o Dysmetria
o Saccadic Eye movement
o Titubation
o Truncal swaying
o Dysdiadokinesia
 o Speech patterns
o Romberg’s Test: cerebellar vs sensory
o Lateralization

Coma

- A state of unarousable unresponsiveness in which the patient has no evidence of self or

environmental awareness
- Considered a medical emergency
- Causes
o Traumatic- contusion, intracerebral hemorrhage, diffuse axonal injury
o Metabolic- Diabetes, thyroid diseases, acid-base-electrolyte imbalances, hypoxia,
hepatic/renal/adrenal abnormalities, thermal abnormalities
o Vascular- CVA, SAH, Aneurysm, hypertensive encephalopathy, eclampsia
o Infectious- Meningitis, abscess, subdural empyema, Enhcephalitis
o Toxic- Poisoning, overdose, withdrawal syndromes
o Structural- Tumor
o Psychogenic- Conversion reaction, depression, catatonia, malingering

Paresthesia and dysesthesia

- Symptoms of peripheral nerve dysfunction caused by ectopic nerve impulses and

generated in these fibers
- Paresthesia: experienced in the absence of any specific stimuli
o Dysesthesia: results of specific stimulus
- Sensory Phenomena

Positive Phenomena Negative Phenomena

- Includes tingling, pins and needles,
prickling bandlike sensation, lightning
shooting sensation (Lacinations),
aching, drawing, pulling, crawling,
tightening, burning, searing, electrical
and raw
- Pain may or may not be perceived
- Not always accompanied by sensory
deficit on exam
- Describe a decrease or loss of feeling in
a particular distribution
- Generally accompanied by abnormal
findings
- Hypoesthesia, analgesia, hyperesthesia,
hyperpathia
- Other negative symptoms: dry skin,
motor weaknesses, orthostatic,
autonomic dysfunction, cold
extremities

Diagnostic Procedures in Evaluating Clients with Neurologic Problems

Radiologic Examinations

- Radiogram: AKA X-rays, Roentgenogram

- Plain FILMS:
o Uses external beams
o Performed without contrast media or augmentation with other techniques
o Skull-Films
 Radiographic examination of the cranial vault and facial bones
 Potential identification of Fractures, tumors and Changes in bone structure
and Size
 “normal skull, facial and jaw bones: normal brain tissue: normal suture
lines and fontanels in infants”
 Contraindications
 Pregnancy: Unless benefits of performing procedure greatly
outweigh the risk to the fetus
 Nursing Responsivities (prior to procedure)
  Explain to the client, prior to procedure: Painless, length of the
procedure, nonindication for NPO and sedation
 Teach: to remain still during procedure
 Assess: Baseline Neuro Check and VS, Metal prostheses, Jewelry,
Eyeglasses, other metal objects, LMP
 Nursing Responsibilities (After the Procedure)
 Reassess: Neurocheck and compare with baseline, presence of
complications (Fractures and injuries)
o Spine Films
 Examinations of various segment of the spine
 Usually indicated for clients experiencing pain and suspected Spinal Cord
Injury (SCI)
 “normal vertebral bodies: no abnormal curvatures or fractures of the
spine”
 Contraindication and Nursing Care: same as Skull films

Computer Tomography Scanning

- Uses Narrow X-rays beams to scan body parts in successive layers to provide cross-
sectional views of the brain, distinguishing differences in tissue densities of the skull,
cortex, subcortical structures and ventricles
- Provides faster and safer diagnosis
- May use iothalamate meglumine per IV as contrast medium if a tumor and other
pathologies causing BBB damage is suspected
- Usually indications
o Early detection of MS
o Determination of the cause of increased ICP (tumors)
o Diagnostic for Stroke
 Cerebral infarction vs hemorrhage
 Size and location of a lesion causing a stroke
o Detection of presence of brain infection or inflammatory condition such as an
abscess or necrosis
- “normal size, shape and position of intracranial contents: no tumors, hemorrhage,
aneurysm, infarction, infection, ventricular or tissue displacement, enlargement or
congenital abnormalities”
- Contraindications
o Pregnancy
o Allergy to iodine, if contrast medium is to be used
o Extreme claustrophobia that prevents the client from lying still, unless medication
are to be given prior to procedure
o Unstable medical status
- Nursing responsibilities (prior)
o Explain the procedure, length of the study, cooperation
o Assess for claustrophobia, LMP, baseline VS
o If with contrast medium
 NPO 6-12 hrs
 Assure presence of an access and hydration
 Assess for S. Creatinine and allergy to iodine
- Nursing responsibilities (post)
o Perform neurochecks
o Hydrate client well

Magnetic Resonance Imaging (MRI)

- Uses magnets to cause hydrogen nuclei (protons) to align in body parts, to be detected by
radiofrequency pulses
- Used most commonly to evaluate the nervous and musculoskeletal system
 - Can detect chemical changes within cells
- May use a paramagnetic contrast medium (Gd-DTPA) that could cross the BBB to
enhance imaging
- Indications
o Diagnosis of brain tumor, stroke and MS without exposure to ionizing radiation
- “normal anatomic structures: soft tissue density: and blood flow rate of head, face,
nasopharynx, neck and tongue, and brain: no pathology such as masses, lesions, infarcts,
hemorrhage, aneurysm, hematomas, edema or demyelination of nerve fibers”
- Contraindications
o Pregnancy
o Extreme obesity
o Unstable medical status
o Extreme claustrophobia
o Cardiac pacemaker: deactivation
o Metallic clips, prostheses, heart valves: displacement and injury
- Nursing Care
o Almost the same as CT scan
o Teach: stay still and cooperation, thumping sounds, length of procedure
o Assess: metal implants: pacemaker, prostheses, aneurysm clips

PET and SPECT

- PET: positron Emission tomography

o Useful in determining dopamine, serotonin, acetylcholine
- SPECT: single photon emission computed tomography
o Useful in determining dopamine levels
- “normal blood flow and metabolism in body tissue: no patter that reveal organ
abnormality”
- Contraindication: pregnancy
- Nursing Care:
o Teach: length of procedure
 Restrict smoking, alcohol or caffeine-containing beverages for 24 hours
prior to study
 Restrict medication (tranquilizers)
 Use of blindfold and earplugs is used

Cerebral Angiogram

- X-ray visualization of the cerebral blood vessels and the carotid and vertebral arteries
after injection of an iodinated contrast medium via catheterization of the femoral (most
common site), the carotid, or the brachial artery.
- Aids in the diagnosis of Cerebrovascular abnormalities
- “normal structures and patency of cerebral vessels and carotid and vertebral arteries: no
evidence of cerebral aneurysm, plaques, or spasms: thrombosis: fistulae: tumor: AV
malformations: or hematoma
- CI
o Pregnancy
o Allergy to iodinated contrast medium, unless prophylactic medication are
administered or nonionic dye is used for those suspected of iodine sensitivity
o Presence of bleeding disorder
o Acute or severe renal or hepatic disease
- Nursing responsibilities (prior)
o Secure written consent
o Assess for allergies, S. creatinine
o Place client on NPO for 4-8 hours
o Shave insertion site
o Remove metals
 o Take Baseline VS, check and mark peripheral pulse
o Premedicate as ordered
- Nursing responsibilities (post)
o Check and prevent bleeding
o Do neurovascular checks (6-P’s)
o Promote dye excretion

Myelography

- Allows visualization of the spinal subarachnoid space or the spinal canal to determine
abnormalities
- A contrast medium is injected into the spinal canal via lumbar puncture
- Series of X-rays is obtained simultaneous to injection of dye
- “normal structure of the subarachnoid spaces of the spinal column: no spinal
abnormalities or obstructions”
- Indications
o Suspected congenital abnormalities or injuries
o Detection of lesions of the spinal column
o Detection of bone structure changes in the spinal column
o Aid in diagnosing chronic back pain etiology
- Contraindications
o Pregnancy
o Known allergy to iodine or iodinated contrast media
o Suspected or confirmed increase in ICP
o Infection at the puncture site
- Nursing Responsibilities (prior)
o Assess: increased ICP, allergies, puncture site, VS
o Teach: NPO for 8-12 hours, headache may occur
o Administer: laxative or enema, sedatives as ordered
o Shave puncture site as necessary
- Nursing Responsibilities (post)
o Positioning
 Water soluble dye: elevate HOB (semi fowlers)
 Air: Trendelenburg
 Oil soluble dye: flat on bed for 8 hours
o Monitor neurocheck, VS, complications (Reaction, meningitis)
o Encourage fluid intake
o

Lumbar Puncture (spinal Tap)

- Insertion of a spinal needle into the subarachnoid space (usually between L3-L4) to
withdraw CSF for examination, measure CSF pressure, determine spinal subarachnoid
blockage and administer antibiotic intrathecally
- CSF analysis
o Pressure: 70-200 mmH2O
o Cell count: free from RBC
o CHON: 15-45 mg/dL
o CHO: 40-80 mg/dL
- Contraindications
o Infection at site
o Elevated ICP
- Queckenstedt’s Test
o Lumbar manometric test
o Assessment for blockage in the subarachnoid pathway
o Done by compression of the jugular veins on each side of the neck during LP
o Normal: rapid rise in CSF pressure
 o Partial blockage: slow rise in CSF pressure
o Complete blockage: no pressure change
- Nursing care (Prior)
o Secure consent
o Teach: positioning, remaining still, not to bear down, local anesthetic
o Prepare: void, hospital gown
- Nursing (post)
o Assess for brainstem herniation and meningeal irritation
o Position: flat on bed for 6-8 hours
o Liberal amounts of fluids

Electromyography (EMG)

- “Normal muscle electric activity during rest and contraction states, no neuromuscular
disorder or primary muscle diseases”
- Contraindication
o Medication regimen that includes anticoagulant therapy
o Infection at or near the site of electrode placement
- Electrophysiologic study performed to determine the electric activity of specific muscles
assist in the diagnosis of muscular disease and the effects of other diseases on muscles
- A 24- gauge needle containing fine wire electrode is inserted into the muscle to detect
electric potentials, which is then amplified, fed to a loudspeaker, displayed on a screen in
wave forms and recorded on magnetic tape
- Nursing Care (prior to procedure)
o Secure signed written consent
o Teach: discomfort of the procedure, avoid cigarette smoking and caffeine
beverages 3 hours prior to procedure
o Administer premeds (analgesic) as ordered
- Nursing Care (after)
o Remove electrodes and cleanse skin
o Assess site for hematoma & inflammation, and administer analgesic as prescribed

Electroencephalography (EEG)

- Electrophysiologic study performed to measure the electric activities of the brain cells
- Electrodes are placed on the scalp which will record brain waveforms during sleep and
waking periods to reveal patterns characteristics of specific disorders
- “normal brain structures and function: electric activity characteristics with waveforms
that indicate normal EEG signals in frequency and amplitude”
- Nursing Care
o Drugs/food that may alter neuro-stats are withheld 24-48 hours prior to procedure
o Time: 45-60 minutes (12 hours for sleep EEG)
o Shampoo (before and after the procedure
 Collodion glue: Acetone

Others

The Cerebrum

- 2 hemispheres separated at the great longitudinal fissure by the falx cerebri, joined at the
corpus callosum
- GYRI: convolutions to increase brain’s surface area
- Cerebral Cortex: external portion (2-5 mm depth) made up of gray matter

Blood-Brain Barrier
 - Barrier formed by endothelial cells of brains capillaries with continuous tight junction
impenetrable to many substances (e.g. macromolecules and drugs) that circulate in the
blood plasma
- Maintained by the astrocytes
- Can be altered by trauma, cerebral and hypoxemia
- Ammonia, bilirubin, Carbon monoxide and Lead, Ketonesuu

Parietal Lobe

- Sensory Lobe
- Analyses and relays interpretation of information to other cortical areas

The Brain stem

- Mid Brain
o Connects the pons and the cerebellum to the cerebral hemisphere
o Contains center for auditory and visual reflexes
o Origin of CN 3 & 4

Cerebrospinal Fluid

- Clear, colorless, 100-160 mL

- Pressure: 75-180 mm H2O, 0-15 mmHg
- Glucose: 50-80 mg/dL
- Protein: 20-50 mg/dL
- Lateral ventricles (choroid plexus)- Foramen of Monro- Third ventricles- Aqueducts of
Sylvius- Fourth ventricle- Foramen of Luschka/Magendie- Subarachnoid space (Cisterna
Magna)- Superior sagittal Sinus(arachnoid villi)

Cranial Nerves

Cranial Nerves Functions Deviations

I. Olfactory Smell Anosmia
II. Optic Vision Altered vision
III. Oculomotor Pupillary constriction, upper Anisucuria
lid elevation
IV. Trochlear Eye movement (superior Nystagmus
oblique)
V. Trigeminal Mastication, Sensation of Tic Douloreux
face and cornea
VI. Abducens Eye movement (lateral Diplopia, Ptosis of the
rectus) eyelids
VII. Facial Bell’s palsy, Ageusia
VIII. Vestibulocochlear Tinnitus, Vertigo
IX. Glossopharyngeal Ageusia, dysphagia
X. Vagus Loss of gag reflex,
bradycardia, increase HCL
production
XI. Accessory Inability to move the
shoulders
XII. Hypoglossal Inability to rotate or move
the shoulders, deviation of
the tongue to one side of the
mouth

Neurologia

- Oligodendrocytes
 o Produce and maintains myelin sheath around several adjacent axons of CNS
neurons
- Schwann cells
o Produces and maintain myelin sheath around single axon of an PNS neuron
o Participate in the regeneration of PNS axon
- Smaller, 5-50x in number, half volume of the CNS
- Supports, nourish and protect neurons
- Do not generate or conduct impulses
- Can multiply and divide

Major Neurotransmitters

Neurotransmitter Source Action

Acetylcholine (major
transmitter of the PNS)
Serotonin
Dopamine
Norepinephrine (major
transmitter of the SNS)
Gamma-aminobutyric acid
(GABA)
Enkephalin, endorphin
Histology of the Nervous Tissue
Many areas of the brain,
autonomic nervous system
Brain stem, hypothalamus,
dorsal horn of the spinal cord
Substantia nigra and basal
ganlia
Brain stem, hypothalamus,
postganglionic neurons of the
SNS
Spinal cord, cerebellum, basal
ganglia, some cortical areas
Nerve terminals in the spine,
brainstem, thalamus and
hypothalamus, pituitary gland
Usually excitatory,
parasympathetic effects
restrain (stimulation of the
heart by vagal nerve)
Restraining, helps control
mood and sleep, inhibits pain
pathways
Usually restraints, affects
behavior (attention, emotions)
and fine movements
Usually excitatory, affects
mood and overall activity
Excitatory amino acid

The Neurons

- Classified according to Morphology depends on number of processes extending from cell

body
o Multipolar: several dendrites and one axon
o Bipolar: one main dendrite and one axon
o Unipolar: dendrites and axon fused together to form a continuous process
- Primary functional unit of the nervous system
- Possesses Electrical excitability: ability to response to stimulus and convert it to action
potential (impulse)
- Cell body
o Contains nucleus and cytoplasm with organelles
o Site of synthesis of most cellular molecules needed for a neurons operation
- Dendrites
o Receiving/input parts of the neuron
- Axon
o Conducts impulses away from cell body
o

The Spinal Cord

- Connection between brain and periphery

- Continuous structure of the medulla, extending from the foramen magnum, to the upper
boarder of L2
o Approximately 45 cm (18 inches) long
 - Tapers down to the CONUS, MEDULLARIS, continuing to the nerve roots extending
below it called CAUDA EQUINA
- Consists of an inner gray matter and an outer white matter
- Protected by meninges
-

Nervous System

Peripheral NS Central NS

Autonomic NS Somatic NS Brain Spinal Cord

Sympathetic NS Para Sympathetic NS Forebrain Midbrain Hindbrain

Telencephalon Diencephalon Mesencephalon Metencephalon Myelencephalon

Cerebral Cortex Thalamus TectumPons Medulla

Basal ganglia Hypothalamus Tegmentum Cerebellum

Hippocampus

Amygdala

Delirium
- A condition involving an acute
confusional state recognized by the
patient’s change in consciousness,
attention, cognition, perception or
psychomotor activity
- Acute in onset, often fluctuates widely
throughout the day and is potentially
reversible
Dementia
- Characterized by a progressive
cognitive decline leading to social or
occupational disability occurring in a
state of clear consciousness
- Usually age dependent etiology
- Often irreversible
-

Management of Patient with Neurologic Dysfunction

Intracranial Pressure
- Determined by contents of the rigid skull
o Brain tissue:1,400 mL :Space occupying lesion
o Blood: 75 mL : hemorrhage, AV-mal
o CSF: 75-150 mL : hydrocephalus
o Pressure: 10-20 mm Hg (N=0-15 mmHg-ventriculostomy)
 Position: HOB elevated
- Monro-Kellie hypothesis
o “an increase in any one of the components, causes a change in the others”
- Pathophysiology
o Increased ICP > Attempt at normal regulation of ICP > Slight increase in cerebral
perfusion pressure > if ICP remains high: loss of autoregulatory mechanism >
passive dilation of cerebral vessels > increased blood flow, venous congestion >
further increase in ICP > cellular hypoxia > herniation > Brain Death
- Predisposing factors
o Head injury> scalp, skull or brain
 Cause: V/A, fall
  s/sx: Battle’s sign, Raccoon’s eyes, CSF otorrhea and rhinorrhea (check
halo sign)
 contusion- more severe, he or bruising of the brain
 concussion- mold, jarring of the brain, temporary LOC with no
structural damage- retrograde amnesia (temporal affectation)
 Intracranial hemorrhage- most serious
 Intracerebral hematoma- bullets or missile injury
 Epidural hematoma- skull and dura
o Lucid interval- classic characteristics
o Patient has LOC and followed by interval of apparent
recovery and deteriorates rapidly
o Arterial bleeding- middle meningeal artery- emergency!
 Subdural hematoma- dura and arachnoid or pia
o Venous bleeding- slow
o Acute- major head injury- sx 24-48 hours
o Subacute- sequela of less severe contusion- sx 48-2 weeks
o Chronic- elderly (alcoholic) are prone- brain atrophy due to
aging- sx 3 weeks to months
o Tumor
 Meningioma, gliomas, astrocytoma (glioblastoma multiforme stage 4)
 Surgery
o Supratentorial craniotomy
 Position: semi-fowler
o Infratentorial craniotomy
 Position: flat on bed
 Avoid neck flexion
o Localized abscess
o Hydrocephalus
 Non-communicating (tumor), communicating (damage to arachnoid villi)
 Txt: acetazolamide> decreased CSF production- carbonic anhydrase
inhibitor
 Surgery: vp shunting
o Meningitis
o Cerebral edema
o Hemorrhage (stroke)
- Signs and symptoms
o Early
 Changed or decreased LOC- restlessness to confusion- 1st sign
 Irritability and agitation
 Disorientation to lethargy to stupor to coma
o Late sign
 Changes in v/s (cushing triad)
 Widened pulse pressure- increased systolic BP, same diastolic
 Decreased HR- bradycardia
 Decreased RR- bradypnea
 Cheyne-stokes respiration
 Increased body temperature- late sign!
o Headache, papilledema, projective vomiting
o Abnormal posturing
 Corticated- corticospinal tract
 Decerebrate- upper brain
o Unilateral dilation of pupils
 UNCAL herniation> puts pressure on CN II> unequally pupillary
dilation> anisucuria
o Seizure 24h to 7 days after the injury
o Signs of hypoxia
 Early
  RAT- restlessness, agitation, tachycardia
 Late
 BCDE- Bradycardia, cyanosis, dyspnea, extreme restlessness
- Clinical Manifestation
o Changes in level of consciousness
 Restlessness, agitation, headache, projectile vomiting
o Cushing’s response (reflex) & triad
 Cushing reflex: increased systolic BP, widening of pulse pressure,
bradycardia
 Cushing Triad: hypertension, bradycardia and bradypnea
o Pupillary changes
 Slower responses, unequal pupils, dilation of pupils
o Uncontrolled high temperatures
o Changes in respiration
 Irregular breathing pattern, bradypnea
o Focal signs
 Muscles weakness, paralysis
 Decrease responses to painful stimulus
 Babinski reflex
 Decorticate or decerebrate posturing
o Visual changes
 Decrease in visual acuity
 Papilledema (edema of the optic disk)
o Seizure & behavior changes

Site LOC Pupils, Eyes Respirator Motor VS

y Pattern Activity
Cerebrum Confusion, Normal size, Normal Pronator Normal
drowsy, brisk 2mm drift
appropriate
thought process
Diencephalon Lethargy, Stupor Small Eupnea, Hemiplegia Variable
ipsilateral, Cheyne- , decorticate
intact doll eyes Stokes
Midbrain Semicoma Fixed, unequal, Cheyne- Decorticate Widening
nonreactive Strokes, PP, slow
CNH PR
Pons Coma Nonreactive Apneustic Decerebrate Widening
PP
Medulla Coma Fixed, dilated Ataxic Flaccid Increased
BP
- Nursing management
o Maintaining airway and adequate ventilation
 To prevent hypoxia and hypercarbia
 Assist in mechanical ventilation/ambubagging
 Hyperventilate or hyperoxygenate client to 100% before and after
suctioning
 10-15 seconds only
 Elevate HOB 30-45 degrees only
 Not more than 90 degrees
 Provide safety
 Avoid sedatives and opioids>respiratory depression pupil constriction
 Limit fluid intake to 1.2- 1.5 L/day
 Monitor v/s, IO, neurocheck
 Prevent complications of immobility- provide ROM >provide rest
 Manage hyperthermia- decrease metabolic demand
o Prevent increased ICP
 Provide comfortable and quiet environment
  Avoid use of restraints
 Maintain side rails
 Avoid clustering nursing activities
 Avoid Valsalva maneuver
 Avoid straining of stool
 Avoid excessive coughing and sneezing
o Open mouth
 Avoid vomiting> NGT insertion
 Avoid bending, stooping, lifting heavy objects
o Positioning
 Raise head of bed 15-30 degrees
 Keep patient’s head in neutral position (avoid head rotation, neck flexion)
 Avoid use of footboards and hip flexion
o Movement
 Keep client still as much as possible
 Avoid restraints
 Use log rolling technique, keeping head neutral
 Instruct client to exhale during turning
o Hypoxia
 Administer O2 as needed
 Soft nasopharyngeal Airway is preferred than oropharyngeal
 Avoid sedation
o Suctioning
 Do not suction client unnecessarily
 Hyperventilate client before and after suctioning
 Suction no more than 15 secs
o Noise
 Keep environment as quiet as possible
 Before performing procedure, make sure equipment is out of the way
 Restrict conversation in client’s room
 Talk to client (only if necessary) in a low, soothing vice, let familiar faces
talk to patient
o Valsalva Maneuver
 Instruct client to avoid straining at stool
 Omit coughing from usual exercises
 Avoid nausea and vomiting
o Pain, discomfort, nontherapeutic Touch
 Limit or consolidate painful procedures
 Limit nontherapeutic touch (e.g. BP cuffs and O2 tubing)
 Cluster nursing care at intervals to allow periods of uninterrupted rest
 Never startle a client, explain the procedure
o Fever
 Keep client uncovered or if needed use light sheets
 Administer antipyretics as prescribed
o Other specific management
 Control hypertension
 Fluid restriction, regulate IV
 Pharmacotherpay
 Diuretics (mannitol, furosemide)
 Dexamethasone
 Anticonvulsants (diazepam, phenytoin, phenobarbital)
 Surgical management
 Craniotomy
- Medical management
o Osmotic diuretic
 Mannitol- DOC
 Check BP>hypotension
 Strict I and O monitoring
  Administer Via piggy-back (PNSS)- No glucose- containing-
crystallization
 Regulate at fast drip
 N- flushing sensation
 Loop diuretic
 Furosemide
o Administer at am- 10-15minutes- minimum: 6 hours- peak
o Check BP
 Anticonvulsant
 Benzodiazepines- doc
 Do not affect ICP or CPP

Seizures
- Results of abnormal paroxysmal electrical discharges in the cerebral cortex, which then
manifest as an alternation in sensation, behavior, movement, perception and
consciousness
- Epilepsy
o Syndrome of recurrent, idiopathic seizures
o Ultimate cause is unknown
- Types of seizures
o Grand Mal Seizures (Big sickness)
o Petit Mal (Little sickness or absence seizure)
o Psychomotor seizure
o Myoclonic seizure
o Focal motor
- Phases of seizures

A. Prodrome Changes in emotions (anxiety,

depression)
B. Aura Brief sensory experience (epigastric
pain)
Localize area
Temporal – odors
Occipital- bright, flashing lights
Parietal- numbness and tingling

C. Epileptic cry Caused by thoracic and abdominal

spasm
D. Ictus Seizure
E. Post-Ictus Changes in consciousness, behavior,
activities
Grand Mal Seizures

Etiology Characteristics S/Sx Aura Postictal

Most common Most dramatic, Aura, Cry, Present Present
generalized LOC, Fall, Flashing Lights Need for sleep
(w/LOC) TC Smell h/a- common
movement, Spots before Eyes complete
incontinence, Dizziness amnesia
hands
clenched,
pupils dilate
Petit Mal Seizures
Onset Characteristics S/Sx AURA POSTICAL
- Childhood, - Brief Eyes NONE
adolescence periods of focused - Occurs
(decrease altered straight w/o
 frequency in conscious ahead, warning
aging) ness (5- motor
- Idiopathic 30 secs) activity
- NO LOC ceases,
loss of
muscle
tone
Jacksonian or Focal
Seizure
w/ structural brain Depends on the Begins in PRESENT PRESENT
disease (motor site (progressive) hands, foot or numbness,
cortex/posterior face and may tingling, crawling
frontal lobe) end in grand
mal seizure
Psychomotor seizure
(devil possessed)
Any Age Sudden change in Partially Present PRESENT
Temporal lobe awareness w/ conscious, De Javu Contusion
distortion of psychic sx, Amnesia
feelings and intoxicated, Hallucinations Need for sleep
thinking antisocial acts
Longer than petit (violent), Illusions
mal automatism,
chest pain,
respiratory
distress,
urinary
continence
- Partial seizure
o Partial Seizure- s/sx
o Simple w/o LOC
 Fingers may shake
 Mouth may jerk
 Talks unintelligently
 Dizziness
o Complex w/LOC
 Motionless
 Fear, anger, irritable
 Does not remember
- EEG
o A record of electrical activity patterns of the brain, made with scalp electrodes in
the form of wave patterns
o Limited value for young children
o absent – brain death

Alpha O Wakefulness
Beta F
Delta Deep sleep
Theta T Drowsy
o INTERVENTIONS:
 Explain purpose (painless)
 Instruct s.o. to minimize sleep the night before
 Discontinue tranquilizers, anticonvulsant
 Avoid stimulants and alcohol
 No dietary restrictions – hypoglycemia
- Complications:
o Status epilepticus
 Continuous seizure, rapid in succession (30 mins)
  If not treated – irreversible brain damage (inadequate glucose and O2)
- Causes
o Intoxications
 Cocaine, lithium, lidocaine, theophylline, heavy metal poisoning
o Infections
 Septic shock, bacterial or viral meningitis, brain abscess
o Ischemia
 CVA, TIA (common cause of seizure in elderly clients)
o Intracranial pressure
 Increased ICP
o Metabolic and electrolytes disturbances
 Hyponatremia, water intoxication, hypoglycemia, hypocalcemia, uremia,
thyroid storm, hyperthermia
o Mass lesions
 Brain metastases, primary brain tumor
o Missing Drugs
 Noncompliance with anticonvulsants in client with epilepsy
 Acute withdrawal from alcohol, benzodiazepines, barbiturates
o Miscellaneous
 Pseudo seizures
 Not actual seizures (of psychiatric origin)
 Distinguishable via an EEG
 Eclampsia
 Preeclampsia + seizure
 Definitive treatment: delivery
 Treatment of choice : Mg infusion
 Hypertensive encephalopathy
- Types
o Partial Seizures
 Begins with one part of the brain (typically temporal)
 Initially produce symptoms that are referable to the regions of the cortex
 Types
 Simple partial seizure
o Consciousness remains intact
o Seizure may remains localized
o May evolve into complex partial seizure
o May involve transient unilateral clonic-tonic movement
 Complex partial seizure
o Consciousness in impaired
o Postictal confusion
o Automatism (for 1 to 3 mins): purposeless, involuntary,
repetitive movements
o Olfactory or gustatory hallucination
o Generalized seizure
 Involves disruption of electrical activity in the entire brain
 Characterized by loss of consciousness
 Types
 Tonic-clonic (grand mal) seizure
o Bilaterally symmetric and without focal onset
o Aura may be experienced
o Begins with sudden loss of consciousness- a fall to the
ground
o Tonic phase: rigidity, trunk and limb extension, apneic
o Clonic phase: musculature jerking of the limbs and body
for at least 30 secs
 o Patient becomes flaccid and comatose before regaining
consciousness
o Postictal confusion usually 10-30 mins
o Other features: tongue biting, apnea and incontinence
 Absence (petit mal) seizure
o Typically involves school-age children, usually resolving as
a child grows older
o Patient seems to disengage from current activity
 “stares into space” then returns to activity
 “absent minded” during episodes
 Confused with “day dreaming”
o Episodes are brief (few secs) buy may reach 100x a day
o Impairment of consciousness but no loss of postural tone,
or continence and no postictal confusion
o Minor Clonic activity: blinking and head nodding
- Diagnosing
o Known Epileptic
 Check anticonvulsant levels (narrow therapeutic window)
o Unclear history
 CBC, electrolytes, blood glucose, LFT, RFT, UA
 EEG: most helpful diagnostic, but alone is inadequate
 Normal EEG in first timers: lower risk for recurrence
 CT scan, MRI to identify structure lesions
 LP and blood cultures (if febrile)
- Treatment
o Anticonvulsant agents  act on the cerebral cortex; non selective
 Phenytoin sodium (Dilantin)
 s/e GANDA / BANDA
 gum tissue growth  gingival hyperplasia – soft toothbrush only!
 Bone marrow depression  anemia, leukopenia,
thrombocytopenia
 Ataxia, anorexia  adequate nutrition, take with meals
 Nystagmus (toxicity)
 Discoloration of urine – pinkish or reddish
 Arrhythmia (monitor HR)
 HEALTH TEACHINGS
o Take at the same time with milk and food
o Taper drug slowly
 Phenobarbital (Luminal) – drowsiness - depress consciousness
 Diazepam (Valium) – respiratory depression
 Carbamazepine (Tegretol) – agranulocytosis
 Partial and Grand Mal, Seizures
 DOC: phenytoin, carbamazepine
 Other options: phenobarbital, valproate, primidone
 Petit Mal
 Ethosuximide and valproic acid
- Nursing Interventions:
o BEFORE
 Privacy
 Lie on floor, turn head to left side
 Protect head, loosen clothing
 Raise side rails
 Do not open jaws
 Do not insert anything
 Do not restrain
o DURING
 Nothing!!!
 o AFTER
 Side lying
 Re-orient
 Becomes agitated
- Care for seizing client
o Observation and documentation of patient signs and symptoms before, during and
after seizure
o Nursing action during seizure focus on patient safety and protection
o After seizure care, prevent complications
o Process
 Cushion head, Loose necktie, turn on side, nothing in mouth, look for ID,
don’t hold down, as seizure ends, Help
- Primary Prevention
o Patient education:
 Advise to have ID to identify himself as an epileptic
 Educate about medications and course of treatment
 Adequate rest, regular meals, well-balanced diet must be emphasized
 Avoidance of extreme physical exertion, fatigue, infection, fever, and
emotional stress – triggering factors
 Avoid dangerous activities
 Alcohol is contraindicated
 Avoid stimulants

Altered Level of Consciousness

- Level of consciousness is a measurement of a person’s arousability and responsiveness to
stimuli from the environment
- An altered level of consciousness is any measure of arousal other than normal
- Associated with ALOC
o A- Acidosis, alcohol
o E- epilepsy
o I- infection
o O- overdose
o U- uremia
o T- Trauma, tumor
o I- Insulin
o P- Psychosis
o S- Stupor
- ALOC7
o Conscious
 Normal
 Oriented 3x, responds prompt, spontaneous and correct
o Confused
 Obtuse
 Disorientated, impaired thinking and response
o Delirious
 Disorientated, restlessness, hallucinations and sometimes delusions
o Somnolent
 Drowsy/sleepy
 Responds to stimulus with only mumbles and disorganized movements
o Obtunded
 Decreased alertness
 Decrease interest in environment, slowed responses and sleepiness
o Stuporous
 Sleep-likes state (not unconscious)
 Only responds by grimacing or withdrawal to painful stimuli
- Diagnosing
 o Ineffective airway clearance
o Risk for injury
o Deficient fluid volume
o Impaired oral mucous membrane
o Risk for impaired skin integrity
o Impaired tissue integrity of the cornea
o Ineffective thermoregulation
o Impaired urinary elimination (retention or incontinence)
o Bowel incontinence

Cephalgia
- Headache
- Primary Headache
o Diagnosis is based on the characteristics clinical history and elimination of other
pathologies such as stroke, intracranial bleed, AVM, or brain tumor
- Secondary headache
o Due to neurologic or systemic disease
- Migraine
o Inherited disorders (probably an autosomal-dominant trait)
o Pathogenesis is not clearly defined
 Serotonin depletion plays a major role
o More common in women than in men
o More common in those with a family history
o Typically occurs in 1-2x a month
o Pain, nausea and visual changes are typical of classic form
o Types & triggers
 Classic migraine
 Migraines with Aura
 Aura is usually visual, but can be neurological
 Common Migraine
 Migraine without Aura
 Menstrual Migraine
 Occurs between 2 days before menstruations and the last day of
menses
 Similar treatment + estrogen support
 Status Migrainous
 Last over 72 hours and does not resolve spontaneously
o Migraine headache triggers
 Foods containing Amines
 Cheese
 Chocolate
 Nitrates
 Processed lunch meat
 Hot dogs
 Smoked meat
 Containing
 Vinegar
 Onions
 Monosodium glutamate
 Fermented or marinated
 Caffeine
 Nicotine
 Ice cream
 Alcohol
 Emotional stress
 Fatigue
 o Manifestations
 Prodromal phase
 Consist of symptoms of excitations or inhabitation of the CNS
 Elation, excitability, increased appetite, craving for certain foods
(especially sweets)
 Depression, irritability, sleepiness, fatigue, may be manifested
 May precede the actual migraine attack by up to 24 hours
 Severe throbbing unilateral headache
 Last for 4-72 hours
 At the times may be generalizable over the entire head and may
last for days if not treated
 Pain aggravated by coughing, physical activity, or bendin dow
 Variable pain quality “throbbing” or “dull and achy”
 Others symptoms: nausea, vomiting, photo-phono phobia, increased
sensitivity to smell
o Management
 Provide restful environment with decreased stimuli
 Stress therapy and relaxation techniques
 Diet: small frequent meals
 Avoid: chocolate, nuts, onions, seasonings, cheese, citrus, coffee, dairy
 Pharmacotherapy
 Beta-blockers
 CA- Channel blockers
 TCA: tofranil, Elavil
 Ergotamine Tartrate
 NSAIDs
 Opioids Analgesics
- Tension headaches
o Related to stress and muscle contraction
o Unknown (may be similar to migraines)
o Usually worsens throughout the day
o Precipitants
 Anxiety
 Depression
 Stress
o Often confused with mild migraine
o Tension pain is like a band squeezing the head
o Manifestation
 Pain is steady, aching and encircles the entire head (tight band-like pain
around the head)
 Usually generalized but may be the most intense around the neck
or back of the head
 Can be accompanied by tender muscles (posterior cervical,
temporal frontal)
 Tightness in posterior neck muscles
o Management
 Attempt to find the casual factors
 Evaluate patient for possible depression or anxiety
 Stress reduction
 Pharmacotherapy
 NSAID, acetaminophen, ASA: standard treatment for mild-
moderate HA
 Severe HA: migraine meds
- Cluster headaches
o Very rare- though to be a variant of migraine
o Usually occurs in middle-aged men
 o Subtypes
 Episodic: 90%
 Last 2-3 months
 With remissions of months to years
 Chronic: 10%
 Last 1-2 years
 Does not remit
o Cluster: pain is in and around one eye
o Manifestations
 Excruciating periorbital pain (“behind the eye”)
 Almost always unilateral
 Deep, burning, searing, stabbing
 Usually begins few hours after sleeping and last for 30-90 minutes
 Occurs nightly for 2-3 months then remits (months to yrs)
 Worsens with alcohol and sleep
 Accompanied by ipsilateral lacrimarion, facial flushing, nasal stuffiness,
discharge
o Management
 Acute attacks
 DOC: sumatriptan (imitrex)
 O2 inhalation
 Prophylaxis
 DOC: Verapamil
 Alternative agents
o Ergotamine
o Methysergide
o Lithium
o Corticosteroids

Management of Patient with Cerebrovascular Accident

Cerebrovascular accident

- Stroke, Apoplexy, Brain Attack

- Syndrome of persistent neurologic dysfunctions related to cerebral infarcts caused by
decreased cerebral blood flow
- Epidemiology
o Third most common cause of death in the US
o Leading cause of disability
- Types
o Ischemic
o Hemorrhagic

Ischemic Stroke

- Classes
o Transient Ischemic Attack (TIA)
 Neurologic deficits that last from a few minutes to no more than 24 hours.
o Reversible Ischemic Neurologic Deficit
 Same as TIA with duration of S/Sx (last 24hours-2 weeks)
o Evolving Stroke
 Stroke that is worsening
o Completed Stroke
 Stroke with maximal deficit has occurred
- Predisposing
o Thrombosis- atherosclerosis
  Most common, gradual onset
 Lacunar Strokes- small penetrating
 Occurs during sleep or rest
 Endarterectomy
o Embolic (cv) > lung or brain
 Pulmonary embolism
 Sudden sharp chest pain
 Unexplained dyspnea or SOB
 Tachycardia, palpitations
 Cerebral embolism
 Headache, disorientation, confusion, decrease in LOC
 MGT: thrombolytic > anticoagulant therapy
o Arterial hemorrhage
 AV malformations. Aneurysm
 Occurs during waking, sudden onset
 MGT: control bleeding > vitamin K
- Risk Factors
o HPN- 1st
o DM
o MI
o Atherosclerosis
o Valvular heart disease
o Lifestyle
 Smoking- nicotine- VC
 Sedentary lifestyle
 Hyperlipidemia- genetic
 Use of contraceptive
 Macro-/mini pills
 Diet
 Emotional stress
 Obesity
- Transient Ischemic Attack
o May not be distinguishable from complete CVA at onset
 Duration of symptoms is the determining difference
 Symptoms are “transient” since reperfusion occur, either because of
collateral circulation or blocking up of the obstruction
o Blockage does not lasts long enough to cause infarction
o Causes
 Embolus
 Hypotension + carotid stenosis (>75%)
o Risk for stroke increase with TIA
- Ischemic Stroke: Risk Factors
o Age and HPN: most important risk factor
o Other risk factors
 Smoking, DM, hyperlipidemia, A. Fib, CAD, FHx, previous
stroke/TIA/Carotid bruits
o Younger Adults
 Oral contraceptive use, hypercoagulable states, polycythemia vera, sickle
disease, vasoconstrictive drugs
- Causes
o Embolic: most common etiology of ischemic stroke
 Possible origins: heart, internal carotid artery, aorta, paradoxical (in
peripheral veins)
o Thrombotic
 Atherosclerotic lesions may be in large arteries of the neck or middle-sized
arteries of the brain (usually MCA)
o Lacunar
  Small vessel thrombotic disease (Thickened arterial wall)
 Usually affects subcortical structures (basal ganglia, thalamus, brain stem)
 Predisposing factors: HPN and DM
 “Lacunes”: healed areas or infarct
 Clinical features are focal and usually contralateral pure motor or pure
sensory deficits
 4 major syndromes
 Pure motor: lesion involves the internal capsule
 Pure sensory: lesion involves the thalamus
 Ataxic hemiparesis: incoordination ipsilaterally
 Clumsy hand dysarthria
- Signs and symptoms
o TIA (Transient ischemic Attack)
 Warning signs of impending stroke, reversible < 24 hours
 h/a- 1st
o Stroke in evolution
 Progression of s/sx- irreversible (38h)
o Complete Stroke
 Stable neurologic s/sx
 h/a
 Cheyne-stokes respiration
 n/v dysphagia
 increased BP
 kernig and brudzinski

- Clinical Features
o Thrombotic Stroke
 Onset: may be rapid or stepwise
 Classically: patient awakens from sleep with neurologic deficits
o Embolic Stroke
 Onset: very rapid (within second), deficits are maximal initially
 Clinical features depends on which artery is occluded

Cerebral Artery Brain Area Involved Signs and Symptoms

Anterior cerebral Infarction of the medial aspect
of one frontal lobe if lesion is
distal to communicating artery:
bilateral frontal infarction if
flow in other anterior cerebral
artery is inadequate
Paralysis of contralateral foot or
leg: impaired gait: paresis of
contralateral arm: contralateral
sensory loss over toes, foot and
leg: problems making decisions or
performing acts voluntarily: lack
of spontaneity, easily distracted:
slowness of thought: aphasia
depends on the hemisphere
involved: urinary incontinence:
cognitive affective disorders

Middle cerebral Massive infarction of most of Contralateral hemiplegia (face

lateral hemisphere and deeper
structures of the frontal,
parietal, and temporal lobes:
internal capsule: basal ganglia
and arm): contralateral sensory
impairment: aphasia:
homonymous hemianopia: altered
consciousness (confusion to
come): inability to eyes toward
paralyzed side: denial of
paralyzed side or limb
(hemiattention): possible
acalculia, alexia, finger agnosia
and left-right confusion:
vasomotor paresis and instability
 Posterior cerebral Occipital lobe: anterior and
medial portion of temporal lobe
Homonymous hemianopia and
other visual defects such as color
blindness, loss of central vision
and visual hallucination: memory
deficits, perseveration (repeated
performance of same verbal or
motor response)

Thalamus involvement Loss of all sensory modalities:

intentional tremors: mild
hemiparesis: aphasia

Cerebral peduncle involvement Oculomotor nerve palsy with

contralateral hemipegia
Basilar and vertebral Cerebellum and brain stem Visual disturbances such as
diplopia, dystaxia, vertigo,
dysphagia, dysphonia
- Diagnostic
o CT (without contrast) of the Head
 First imaging study to obtain
 Done to differentiate a bleed from an infarct
o MRI
 More sensitive than CT scan
 Identifies all infarcts and earlier than CT scan
 Not performed on emergencies
o ECG
o Carotid Duplex Scan
 Assess for carotid Stenosis
o Magnetic Resonance Arteriogram (MRA)
- Management
o Airway maintenance and adequate ventilation
o Restrict fluid intake
o Elevate HOB
o Avoid Valsalva maneuver
o Monitor v/s, I and O, neuro. Check
o PROM exercise q4
o Alternate means of communication
o MEDS:
 Osmotic diuretic- mannitol- DOC
 Loop diuretic- Lasix
 Corticosteroids- dexamethasone
 Mild analgesic
 Thrombolytic- kinase- “tunaw clot”
 Anticoagulants- warfarin (Coumadin)
- Treatment
o Acute
 Treatment of broad efficacy and safety
 Thrombolytic Therapy
 If administered within 3 hours of onset, improved clinical
outcomes seen in 3 months
 ASA
 Best given within first 24 hours, except if in tPA

 Anticoagulants?
 Not proven to have efficacy in acute strokes
 Assess client’s ability to protect airway

Eligibility Criteria for t-PA Administration

  Age 18 or older
 Clinical diagnosis stroke with NIH stroke scale score under
 Time of onset of stroke known and is 3 hours or less
 BP systolic <185: diastolic <110
 Not a minor stroke or rapidly resolving stroke
 No seizure at onset of stroke
 Not taking warfarin (Coumadin)
 Prothrombin time <15 seconds or INR <1.7
 Not receiving heparin during the past 48 hours with elevated
partial thromboplastic time
 Platelet count >100,000
 Blood glucose level between 50 and 400 mg/dL
 No acute MI
 No prior intracranial hemorrhage, neoplasm, AV malformation or
aneurysm
 No major surgical procedures within 14 days
 No stroke or serious head injury within 3 months
 No gastrointestinal or urinary bleeding within last 21 days
 Not lactating or postpartum within last 30 days
o BP control
 In general, do not give antihypertensive unless one of the three conditions
is present:
 Severe hypertension: SBP>220, DBP >120, or MAP >130
 Significant medical condition: AMI, aortic dissection, severe heart
failure, hypertensive encephalopathy
 Thrombolytic therapy: to reduce likelihood of bleeding
o Prevention
 Control of risk factors: HPN, DM, Smoking, Hypercholesterolemia,
Obesity
 ASA
 Surgery (for symptomatic Patients): Carotid Endarterectomy

Hemorrhagic Stroke

Intracerebral Hemorrhage (ICH Subarachnoid Hemorrhage (SAH)

- Bleeding into the brain parenchyma
(66% at basal ganglia)
- Mortality rate: 50% within the next
30 days
- Cause: HPN, cocaine Use (Young
adults)
- S/Sx: abrupt onset of neurologic
deficits (30-90 mins), ALOC,
Increased ICP
- Dx: CT scan
- Mx: BP reduction (gradual),
Nitroprusside, Mannitol
- Bleeding into the CSF- outside the
brain parenchyma
- Mortality rate: 40-50% within the
next 30 days
- Cause: ruptured berry aneurysm,
trauma, AVM
- S/Sx: worst headache, LOC,
Meningeal Irritation, Increased ICP
- Dx: CT scan, LP
- MX: Surgery, Aneurysm clipping,
Analgesia, Decreased ICP, HPN
control: CA channel blockers
(Nifedipine)

Management in Patient with Degenerative Neurologic Disorders

Parkinson’s Disease

- Degenerative disease affecting the extrapyramidal system (EPS

o Results from a loss of dopamine containing neurons
  Nerve cells located in the pigmented substantia nigra
o Essentially a clinical diagnosis
 Brain regions affected by Parkinson’s disease (motor cortex)
- Clinical features
o Personality Changes
 Withdrawal, apathetic, dependent
o Autonomic Dysfunction
 Orthostatic hypotension
 Constipation
 Increased sweating, oily skin
o Dementia in advance stages
o Progressive course
 Significant disability in 5-10 years
- Treatment: NO CURE!

Drug type Function Generic name

Levodopa Enhances conversion of Levodopa (Laradopa)
levodopa to dopamine in Levodopa/Carbidopa
the brain Levodopa/Benserazide
(madopar)
Dopamine agonist Mimics the action of Bromocriptine
dopamine by activating Pergolide
nerve cells in the brain Pramipexole
Ropinirole
Anticholinergic Blocks action of Trihexiphenidyl
acetylcholine, a brain Biperidine
chemical that becomes Benztropine
overactive when dopamine
levels drop
MAO-B inhibitor Blocks action of an enzyme Selegiline
that breaks down dopamine
in the brain
COMT inhibitor Blocks action of an enzyme Tolcapone
that breaks down levodopa Entacapone
in the body, permitting
more levodopa to reach the
brain
Amantadine Stimulates release of Amantadine
dopamine from nerve cells
in the brain and may block
acetylcholine action
- Treatment
o Dopaminergic
 Levodopa, carbidopa-levodopa
 SE: orthostatic hypotension, N/V, Anorexia, Hallucinations, Urinary Color
Changes
 AVOID!!!
 Vitamin B6 (organ meats): Blocks Levodopa
 MAOI’s: HPN Crisis
 Tyramine (aged, smoked, fermented): HPN crisis
o Dopamine Receptor Agonists:
 Pergolide, Bromcriptine, pramipexole
 Controls symptoms and delays need for levodopa
 Useful for sudden episodes of hesitancy or immobility (freezing)
o Anticholinergic
 Trihexiphenidyl (Artane), Biperidine (Akineton), Benztropine (Cogentin)
 Particularly helpful in patient with tremors as major finding
o MAO-B inhibitors
  Selegiline (Eldepryl)
 Inhibits monoamine oxidase B thereby increases dopaminergic activity
o Antiviral (amantadine)
 Transiently increase availability of endogenous dopamine with few side
effects
o Surgery: Deep brain stimulation, thalamotomy, pallidotomy

Myasthenia Gravis

- Autoimmune Neuromuscular Disease

o Antibodies directed against acetylcholine receptors of the neuromuscular junction
resulting to reduced postsynaptic response as manifested by significant muscle
fatigue
 Destruction of acetylcholine receptors
 Destruction of acetylcholine
o Peak incidence
 F: 20- 30 y/o
 M: 50-70 y/o
- Skeletal muscle weakness
o Preservation of sensation and reflexes
o Weakness is exacerbated by continued use of the muscle and improved by rest
o Symptoms worsen by the end of the day
o Ptosis, diplopia, blurred vision: most common initial symptoms
- Acetylcholine Receptor antibodies
o Test of choice (most specific)
- EMG: decremental response to repetitive stimulation
- CT scan to rule out thymoma
- Emergencies
o Myasthenic Crisis
 Diaphragm and intercostal muscle fatigue leading to respiratory failure,
often requiring mechanical ventilation
 Antibiotics (aminogylcosides, tetraacyline), B-Blockers, Antiarrhythmics
(quinidine, procainamide, lidocaine)
o Cholinergic Crisis
 Iatrogenic emergency due to overdosage of cholinergic drugs
 Same symptoms of myasthenia gravis
o Tensilon test (Edrophonium)
 Short acting cholinergic: improvement in muscle strength for 3-5 minutes
in MG
 Improvement: Myasthenic Crisis: give myasthenic medication
 Worsening: cholinergic Crisis: give antidote
- Pharmacotherapy
o Anticholinesterase Drugs: AChE inhibitors
 Pyridostigmine (Mestinon)
 Inhibiting AChE increases concentration of Acetylcholine at the synapse
by decreasing the breakdown of acetylcholine
o Immunosuppressive drugs
 Corticosteroids: if with poor response to AChE inhibitors
 Azathioprine, cyclosporine: third-line agents
o Intravenous immunoglobulin
 Sometimes used for acute exacerbations
- Treatment
o Thymectomy
 Provides symptomatic benefit and complete remission even with absence
of thymoma
 Thymoma is an absolute indication for thymectomy
 o Plasmapheresis
 Remove antibodies to acetylcholine receptors
 Use if all else fail or if patient is on respiratory failure
- Nursing implication
o Administer Medication at exact time!!
o Promote safety
o Prevent aspiration
 Administer meds 20-30 mins ac
 Assess gag and swallow reflex before feeding
 Start meals with cold drinks
o Decrease risk for infection
o Promote rest as necessary

Care for clients with Demyelinating Disorders

Multiple Sclerosis

- Autoimmune disease of unknown etiology causing destruction of the myelin sheath of

nerve fibers (demyelination-plaques)
- Epidemiology
o Incidence is greater at higher latitudes
o F:M ratio 3:1
o Initial presentation 20-30’s
- Signs and symptoms
o Transient sensory deficits
 Decreased sensation or paresthesia in upper or lower limbs
 Most common initial presentation
o Motor symptoms
 Fatigue, weakness, spasticity
o Visual changes
 Optic Neuritis
 Monocular visual loss
 Pain on movement of eyes
 Central scotoma
 Decreased pupillary reaction
 Opthalmoplegia: Diplopia
o Cerebellar involvement
 Ataxia, intention tremors, dysarthria
o Loss of bladder control
o Autonomic involvement
 Impotence, constipation
o Cerebral involvement
 May occur in advanced illness
 Memory loss, personality changes, emotional lability, anxiety and
depression
o S/Sx exacerbated by Heat and Exercise
- Course
o Initial presentation by 20-30’s
 Presents with a localizing deficit such as optic neuritis, one-sided
weakness, or numbness
o Occurs in 4 clinical variants according to progression
o Attack average up to one year
o Prognosis: variable
 Lifespan: often normal
  Diminished quality of life (but not often a debilitating disease)
 Risk for increased likelihood of disability
 Early frequent attacks, onset at older age, progressive course, early
cerebellar or pyramidal involvement
- Diagnosis
o Clinical definite MS
 Two episode of symptoms
 Evidence of two white lesion (imaging or clinical)
o Laboratory-supported definite MS
 Two episodes of symptoms
 Evidence of two white matter lesions on MRI
 Abnormal CSF (Oligoclonal bands in CSF)
o Probable MS
 Two episodes of symptoms and either one white matter lesion or
oligoclonal bands in CSF
o Diagnostic
 MRI; Test of choice
 Most sensitive in identifying demyelinating lesion in CNS
 LP and CSF analysis
 Presence of oligoclonal bands of IgG present in 90% of MS
patients
 Evoked potentials
 Decreased speed of nerve conduction
- Treatment
o Treatment of acute attacks
 High-dose IV corticosteroids can shorten an acute attack
 Dose not alter course of MS
 Most acute attack resolve within 6 weeks
o Disease modifying therapy
 Interferon therapy
 Recombinant interferon B-1a &b
 SE: flu like symptoms
 Started early before disability is irreversible
 Nonspecific immunosuppressive therapy
 Cyclophosphamide: reserved for rapid progressive disease
o Symptomatic Therapy
 Lioresal (Baclofen): for muscle spasticity
 Carbamazepine or Gabapentin for neuropathic pain

Guillain-Barre Syndrome (GBS)

- Infectious polyneuritis, Landry-Guillain-Barre Syndrome, Acute idiopathic polyneuritis

- Acute rapidly progressive and potentially fatal form of polyneuritis causing muscle
weakness and mild distal sensory loss
o Inflammation and degeneration (demyelination) of peripheral motor and sensory
nerves
o Usually preceded by a viral or mycoplasmal infection (of URT or GIT)
- Etiology
o Unknown, probably autoimmune
- Clinical Features
o Abrupt onset with rapidly ascending weakness/paralysis of all four extremities
 Frequently progresses from distal to central
 Frequently progresses to involve, facial and bulbar muscles
 Usually symmetric
 May lead to respiratory arrest if generalized
o Extremities may be painful, but sensory loss is not typical
 o Sphincter control and mentation are typically spared
o Autonomic features: dangerous complications
 Arrhythmias, tachycardia, postural hypotension
o Diagnostic
 CSF analysis: elevated CHON, but normal cell count
 EMG: decreased motor nerve conduction velocity
- Management
o Pulmonary support
 Careful monitoring of pulmonary function
 Mechanical ventilation
o IV immunoglobulin
 If with significant weakness
o Plasmapheresis
 If with progression continues despite IV-Ig
o Do not give steroids!!
 Usually harmful and never helpful

Amyotrophic Lateral Sclerosis (ALS)

- Lou Gehrig’s Disease

- Progressive destruction of upper and lower motor neurons
o Leads to progressive muscle weakness and atrophy
o Etiology: unknown
o Believed to be due to accumulation of glutamate and degeneration of myelin
o Does not involve CN 3, 4 or 6
- Onset: 50-70 y/o
- Prognosis
o 80% mortality rate at 5 years
o 100% mortality rate at 10 years
- S/Sx/Dx
o Progressive muscle weakness
 Usually first noted in the legs or arms
 Spreads to other muscle groups
 No associated pain
 Muscle atrophy
o Muscle cramps and spasticity
o Fasciculation (unnoticed by patient)
o Impaired speech and swallowing
 Dysphagia can lead to aspiration
o Respiratory muscle weakness
 Dyspnea or exertion, and later, at rest
 Orthopnea
 Sleep apnea
 Respiratory failure: End-Stage ALS
o Weight loss and fatigue
o Does not affect:
 Bowel and bladder control
 Sensation
 Cognitive function
 Extraocular muscles
o EMG and nerve conduction
 Confirms degenerations of lower motor neurons
 Can rule out neuromuscular junction disorders
o Clinical or electrical evidence
 Probable ALS: involvement of 2 regions
  Definite ALS: involvement of 3-4 regions (include bulbar, cervical,
thoracic and lumbosacral)
- Treatment
o Mainly supportive
o Riluzole
 Glutamate-binding agent
 May delay death by only 3 to 5 months
o Diazepam/Dantrolene/Baclofen
 For decreasing spasticity
o Quinidine
 Relief of painful muscle cramps
o Respiratory, Speech and physical therapy
o Psychological support
- Nursing/Medical management
o Implement program: foster independence
 Help obtain assistive equipment (walker, wheelchair)
 Assist in hygiene and transfer
 Help client handle accumulation of secretion (suction at home)
 Promote skin care, turn bedridden patients
 Meals: soft solid foods to help dysphagia
 Place client on upright position when eating
 NGT/Gastrostomy if patient cannot swallow
 Provide emotional support

Bell ’s palsy

- Hemifacial weakness/paralysis of muscle innervated by CN 7 due to swelling of the CN

- Prognosis: 80% recover fully within weeks to months
- Etiology
o Uncertain cause
o Possibly viral (herpes simplex), immunologic, ischemic factors
o Often preceded by URTI
- Manifestations
o Acute onset of unilateral facial weakness/paralysis
o Affection of both upper and lower parts of the face
- Diagnosis
o Diagnosis is CLINICAL
o Differentials
 Trauma (temporal bone, forceps delivery)
 Lyme’s disease
 Tumor (acoustic neuroma, cholesteatoma, neurofibroma)
 GBS (usually bilateral palsy)
o EMG
 Consider if paresis fails to resolve within 10 days
- Treatment/Management
o Usually no treatment is required
 Self-limiting: most cases resolve in 1 month
o Short course steroid therapy and acyclovir
 Do not use steroid therapy if considering Lyme’s disease
o Encourage facial exercises
o Eye Care, Oral Care
 Encourage Eye patch at night to prevent corneal abrasion (weakness of the
oblicullaris oculi)
o Meals: chew on unaffected side
o Surgical decompression of CN 7
 Indicated if he paralysis progresses of if continuously deteriorating
Trigeminal Neuralgia (Tic Douloureux)

- Painful sensory disorder of CN 5

o One of the most painful conditions known to mankind
- Etiology
o Unknown cause
o Trigeminal nerve root (at brain stem) compression by intracranial arterial and
venous loops
- Manifestations
o Brief (second to minutes) but frequent attacks of severe, lanciting facial pain
 Involves jaw, lips, gums and maxillary area
 Ophthalmic branch is less commonly affected
 Recurrent attacks may continue for weeks at a time
 No motor or sensory paralysis
- Tx/Mx
o DOC: tegretol (carbamazepine)
 Usually effective in relieving pain
o Other choices: diazepam, baclofen, or phenytoin
 May be in combination with carbamazepine
o Surgery: decompression of the CN
o Meal management
 Liquid/soft diet
 Avoid col/hot foods and drinks
 Chew on unaffected sides

Management of patient with Neurologic Trauma

Head trauma

- Traumatic brain injury (TBI)

- Disruption of normal brain functioning due to traumatic related injury resulting in
compromised neurologic function resulting in focal or diffuse symptoms
- Classifications
o MILD: GCS 13 to 15 with LOC to 15 mins
o Moderate: GCS 9 to 12 with LOC up to 6 hrs
o Severe: GCS 3 to 8 with LOC greater than 6 hours
- Concussions
o Jarring of the brain and against the skull
o Transient period of unconsciousness
- Contusions
o Bruising or extravasation of blood cells
- Lacerations
o Tearing of tissues caused by a sharp object
o Hemorrhage may cause hematoma
- Signs and symptoms
o S/Sx of increased ICP
o S/Sx of basilar skull fractures: CSF leaks, battle’s sign, Raccoon’s Eye
- Nursing care
o Monitor for
 Signs and symptoms of CSF leaks
 Signs and symptoms of increased ICP
  Signs and symptoms of brain steam compression
o Do care for client’s with increased ICP

Spinal Cord Injury

- Trauma causing damage (cutting, pulling, twisting or compression) of any segments of

spinal cord
- Effects are related to loss of function below the level of injury
- Classifications
o Complete transection
o Incomplete transection
- Areas
o Spinothalamic: contralateral
 Pain and temperature
o Fasciculus: Ipsilateral
 Touch, pressure and vibration
o Spinocerebellar: ipsilateral
 For coordinated muscle contraction
- Central Cord syndrome
o Motor deficits (in the upper extremities compared to the lower extremities:
sensory loss varies but is more pronounced in the upper extremities)
o Bowel/bladder dysfunction is variable or function may be completely preserved
o Causes: injury or edema of the central cord, usually of the cervical area
- Anterior Cord Syndrome
o Loss of pain, temperature and motor functions is noted below the level of the
lesion
o Light touch, position and vibration sensation remain intact
o Cause: acute disk herniation or hyperreflexion injuries associated with fracture-
dislocation of vertebra
 It may also occur as a result of injury to the anterior spinal artery, which
supplies the anterior two thirds of the spinal cord
- Lateral Cord Syndrome
o Ipsilateral paralysis of paresis is noted, together with ipsilateral loss of touch,
pressure and vibration
o Contralateral loss of pain and temperature
o Cause: lesion is caused by transverse hemisection of the cord (half of the cord is
transected from north to south), usually as a result of a knife or missile injury,
fracture dislocation of an unilateral articular process, or possibly an acute ruptured
disk.
- Spinal cord
o Areflexia
o Period of flaccid paralysis and a complete loss of all reflexes
 S/Sx: absence of sweating below level of lesion, bowel and bladder
retention, hypotension, bradycardia
 Sx of resolution: contraction of the quadriceps, reflexive, micturition and
defecation, return of sweating
- Autonomic Dysreflexia
o Noxious stimuli: visceral distention, pressure below lesion
o S/sx: severe headache, blurring of vision, hypertension, bradycardia, sweating
above the lesion, pilomotor spasms below lesion
o NxMx
 Check and resolve noxious stimuli
 Place client on sitting position to lower BP
 Hexamethonium Chloride (ganglionic blocker)
 Nitroprusside
MS NOTES