Académique Documents
Professionnel Documents
Culture Documents
CLINICAL EVALUATION OF
HEMIPLEGIA
Dr. S. Aswini Kumar. MD
Anatomy of Brain
2
Fore brain
receiving sensory information from
various sensory inputs of body
processing the information received and
correlating them with prior ones
thinking, perceiving, producing and
understanding language
controlling motor function and autonomic
functions
Mid brain:
auditory and visual responses
Hind brain
balancing equilibrium and co-ordination
Physiology of brain
3
Frontal lobe: Provides executive control over much of the brain's higher functions
Consciousness, self-awareness, judgment, initiation, motivation
Planning, sequencing, word formation, control over emotional responses
Parietal lobe: Perceives, analyzes, and assembles touch information from the body
Integrates visual, auditory, and touch information to formulate complete impression of the world
Left - letters come together to form words and where words are put together in thoughts
Right - recognizing shapes, being aware of one's body in space
Temporal lobe: Hearing, memory acquisition, perception, and categorization of objects
Comprehension of language, listening, reading; music
Occipital lobe: Dedicated entirely to vision
In terms of detection, identification, and interpretation of objects.
Handedness & Contra-laterality of brain control
4
Ophthalmic
artery
Carotid system Internal carotid
Anterior A1 Anterior A2
cerebral communicating
Anterior
choroidal
Anterior limb:
lenticulostriate branches of middle
cerebral artery (superior half)
recurrent artery of Heubner off of
the anterior cerebral artery (inferior half)
Genu:
lenticulostriate branches of middle
cerebral artery
Posterior limb:
lenticulostriate branches of middle
cerebral artery (superior half)
anterior choroidal artery off of
the internal carotid artery (inferior half)
Corticospinal tract
8
When did the event start? When was he last found to be in a normal state?
What is the total duration of the illness? If multiple, of each episode?
What according to the patient or relatives were the initial presenting symptoms?
What was the exact mode of onset; was it abrupt, sudden, sub-acute or gradual?
When was the maximum deficit noted; was it in the beginning or later?
What was the progress of the initial symptoms; static, progressing or regressing?
What were the associated symptoms; in CNS as well as CVS, RES and GIT?
What investigations he has under gone so far and what are the ones planned?
What treatment the patient has received so far and what the ones planned?
History specific for assessing the CNS function
12
Was there any loss of consciousness in the beginning/later; did he recover from it?
Is he able to co-operate in interview and the physical examination?
What is the emotional state of the patient; memory and intelligence?
Is speech affected and if so in what way? Motor, sensory or conductive aphasia?
Which of the cranial nerves are affected and what are the symptoms related?
What is the degree of motor weakness, wasting, flaccidity or stiffness of muscles?
Are all the modalities of sensations normally appreciated or are they abnormal?
Is the patient able to stand with/without support; swaying while standing/walking?
Any symptoms of increased intra-cranial tension like headache or vomiting?
Precise and complete neurological examination
13
Confirms the presence of a stroke syndrome, distinguishes stroke from stroke mimics
Evaluation of level of consciousness and mental status, speech and gait
Cranial nerves, motor function, sensory function, superficial, deep tendon reflexes
Special reference to
Optic fundus - papilledema
III – sign of uncal herniation
VI – sign of increased ICT
Signs of meningeal irritation
Signs of head injury
1. Is the patient having neurological problem?
14
Yes or No?
Or is it only hysterical or malingering?
Is it a medical condition simulating hemiplegia?
Post ictal Todd’s paralysis, episode of multiple sclerosis? ADEM?
If Yes what are the neurological deficits
Hemiplegia, UMN Facial weakness, hemianesthesia, homonymous hemianopia
Dysphasia in a right hemiplegia and dysarthria in a left hemiplegia
Faciobrachial monoplegia
Crossed hemiplegia
Cervical cord lesion?
2. Which are the CNS structures involved?
15
Inspect the face at rest for voluntary & mimetic movements UMN Facial palsy
Examine symmetry of eye blinking and speech motion Upper half of face spared
Ask to raise eyebrows (frontalis) Lower half affected
No Bell’s phenomenon
Close eyes (orbicularis oculi)
Taste not affected
Bell’s phenomenon (Superior rectus)
LMN Facial Palsy
Show teeth (orbicularis oris)
Entire half of face affected
Blow out cheeks (buccinator) Bell’s phenomenon present
Scrunch up nose (nasalis) Other signs of pontine lesion
Retract chin (platysma) Taste affected
4. In what way speech is affected?
17
First test spontaneous speech? – What the patient asks for in the morning – Broca’s aphasia
For tea/food/going to toilet
Now test the comprehension – Whether he understands the meaning of words - Wernickes
Give some simple commands “lift up the unaffected arm” “show the tongue”
Try whether the patient can read aloud? – Pure word blindness
Give a news paper and ask the patient to read aloud from it
Try whether a patient can understand spoken language? – Pure word deafness
inability to comprehend the meaning of speech, but still being able to hear, speak, read, and write.
5. What is the site of localization of lesion?
18
Cortex
Partial deficit, speech involvement, quadrantinopia, cortical sensory, focal seizures
Sub-cortical region
Denser lesion, Full hemiplegia,
Internal capsule
Dense hemiplegia, sparing of speech, absence of speech defects and seizures
Thalamic
Hemiparalysis, hemianopia, hemisensory loss and emerging hyperpathia
Brain stem
Crossed hemiplegia - Nuclear type of cranial nerve lesions + contralateral hemiplegia
6. What is the possible pathology of the lesion?
19
Is it an
ischemic infarct
embolic infarct
hemorrhagic infarct
hemorrhagic transformation of an ischemic infarct
hemorrhage
Is there evidence of significant or dangerous cerebral edema?
Its it a demyelination
Acute Disseminated Encephalomyelitis or Episode of MS
Is it a space occupying lesion: cerebral abscess cerebral tumor, cerebral secondaries
7. Is it an ischemic stroke?
20
Blood supply to part of the brain is decreased, leading to dysfunction of the brain
Cerebral atherosclerosis (producing flow limiting stenosis of a cerebral vessel)
Thrombosis (obstruction of a blood vessel by a blood clot forming locally)
Embolism (obstruction due to an embolus from elsewhere in the body)
Systemic hypoperfusion (general decrease in blood supply, e.g. in shock)
Venous thrombosis (infarcts are more likely to undergo hemorrhagic transformation)
Clinical features
Start suddenly, over seconds to minutes, and in most cases do not progress further
Classically detected by the patient in the morning when waking up
May or may not be preceded by episodes of transient ischemic attakcs
8. Is it a TIA/evolving stroke/completed stroke?
21
Carotid Vertebral
Contralateral weakness Bilateral or shifting weakness
Contralateral numbness Bilateral/shifting numbness
Dysphasia Diplopia
Dysarthria Dysarthria
Ipsilateral mono-ocular Inco-ordination of upper limbs
Contralateral homonymous Ataxia/imbalance/disequilibrium
Combination of above Visual loss in both homonymous ields
10. Is it an Internal carotid artery syndrome
23
Weber Syndrome
Ipsilateral III + Contrlateral HP
Benedicts Syndrome
Ipsilateral III + Weber
Benedict’s