CLINICAL EXAMINATION IN HEMIPLEGIA
Contents
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Introduction
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Clinical examination
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Sensory
system
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Main
points
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General examination
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Reflexes-deep+superficial
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History elicitation
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Higher functions
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Examination
of extrapyramidal system
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Present and past history
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Cranial nerves
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Eamination
of cerebellar system
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Family and personal history
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Spinal motor system
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Other
systems
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I.INTRODUCTION
Hemiplegia is
paralysis of one half of the body-which includes arm, leg and often face on the
affected side.
Terms
used to describe weakness
Hemiplegia:
Total Paralysis on one side of the body
Hemiparesis:
Weakness on one side of the body.
MAIN POINTS: (Hemiplegia)
·
Usually acute in onset
·
Results from upper motor lesion/ most commonly
pyramidal tract lesion
·
Associated symptoms and signs aid the diagnosis
of level of the lesion
·
A detailed history taking is of great value
·
Initially -weakness is flaccid; later-spastic
·
Diagnostic
Features:
Involvement of one half of the body,
hypertonia, hyper-reflexia, extensor
plantar- response and characteristic
hemiplegic gait.
·
Speedy
reach to hospital at the earliest warning signs is a must.
·
Treatment of risk factors- ideal for prevention
·
Refer chart 1 below
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| Main points about Hemiplegia |
II. Points of importance in History
Elicitation (chart2.)
HISTORY
1. Presenting symptoms
·
Motor
symptoms
Decreased movements- Paresis /paralysis
Increased movements; involuntary movements
Feeling of stiffness or flailness
·
Sensory
symptoms
Reduced sensations – hypoesthesia /anesthesia
Increased sensation – occurs in-
Thalamic
pain –where threshold for pain is increased (Hyperpathia)-
-it is a boring, diffuse,
unpleasant and spontaneous pain
-
Exacerbated by touch of clothing –occurs in stroke involving thalamus
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·
H/o
Higher function disorders
Altered consciousness
Speech disturbance
·
cranial nerve Disorders
Especially
VII cranial nerve- (commonest involvement): Lower half of face involved due to
UMN lesion
·
Pearls for
practice:
(Following Activities of daily life affected in
hemiplegia must be asked for in history)
(1. upper limb: using a pen, tying shoe lace,
using comb/tooth brush, dressing
2. Lower limb:
difficulty to lift the foot in front of the other and difficulty in walking
3 Trunk:
Difficulty in turning over in bed, in getting on to bed, in seating himself on
a chair or lavatory seat
Elaboration of presenting complaints
1.
Onset – sudden or insidious
Sudden onset indicates vascular or
traumatic etiology. (Rarely demyelination)
note the time when patient was last found normal
2. Duration
3. Progress- (types)
a.
Stationary or b. progressive with
amelioration later c. rapidly
progressive
d. slowly progressive e. Stuttering
Traumatic lesions are stationary; do not
progress
Vascular lesions progress at first and
then start ameliorating.
Carotid hemiplegia is stuttering in
progress (‘step ladder pattern’)
Malignant lesions are rapidly progressive
Degenerative conditions are slowly
progressive.
4. Rapidity of development of the symptoms-rapid in cerebral hemorrhage
5. Part of the day of development of symptoms –
During sleep / early morning hours –
thrombosis
Day time – hemorrhage or embolism
After exertion –hemorrhage
Accompanying symptoms
Fits,
headache, vomiting, coma –indicate severe hypertension. (h/o hypertension+)
Symptoms
of raised ICT are- headache, vomiting, blurring of vision, fits
Symptoms
of other systems (CVS,
RS, ABDOMEN)
Precipitating factors:
Hemiplegia
precipitated by epileptic fits –Todd’s
palsy.
Precipitated
by fever in – meningitis, encephalitis.
Differential diagnosis to be kept in mind
-Migraine, Todds palsy, TIA,
hypoglycemia,Multiple Sclerosis,hysterical hemiplegia
History of
migraine,fits,hypoglycemia,episodic weakness and relapses of MS,hysteria
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chartHistory elicitation and clinical examPast history
(age of
the patient has a bearing)
·
Elderly: h/o hypertension, diabetes
mellitus, IHD, Hypercholesterolemia,
Recent M.I, Embolic source (cardiac,
artery to artery), large cell arteritis like
giant cell arteritis
·
Young
adults:
1. Cardiac diseases –Mitral stenosis, MVPS, prosthetic valve insertion,
Fallot’s, arrhythmias, cardiomyopathy,
Infective endocarditis
2. Vascular diseases - Hypertension,
collagen vascular diseases
Arteritis –TB, syphilis
3. Hematological: leukemia, lymphoma,
polycythemia, sickle cell anemia
4.
CNS diseases: epilepsy, migraine
5. Respiratory diseases: h/o malignancy,
tuberculosis
6.. Infections: CSOM, cerebral abscess, TB, syphilis
.
·
In females:
H/o oral contraceptives, h/o
recent delivery (which can cause-
-cortical vein thrombosis),
collagen vascular diseases, migraine
·
In infants:
Intra natal and perinatal h/o mother, mile
stones, h/o involuntary -movements
·
In extremes of age: H/o
dehydration (diarrhea, vomiting).-which can predispose to cerebral thrombosis
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Family history
·
hypertension,
diabetes mellitus, ischemic heart diseases,
Epilepsy, migraine
·
Stroke
runs in families but no inheritance-pattern
Personal history
§ Alcoholism,
§ smoking,
§ exposure to toxins,
§ consumption of drugs
§ H/o sexually transmitted
infections/diseases
Alcoholism by definition is the pattern of drinking which is
harmful to the individual and the family
Ill effects of smoking
on CNS: increases the incidence of cerebro vascular lesion.
III.CLINICALEXAMINATION
III.A.GENERAL EXAMINATION
General appearance including posture,motor
activity
Vital signs-Level of
consciousness,pulse,BP,look for pupil size,conjugate deviation of eyes
Meningeal signs
►Neuro
cutaneous markers:
1. Neurofibroma over the skin
(may have associated Tuberous sclerosis of brain)
2. Caféaulait spots-associated
with neuro fibramatosis, tuberous sclerosis, and Ash leaf spots
3. Sebaceous adenoma
4. Sturge Weber syndrome – facial
nevus (port wine stain) involving one half of face with upper eyelid -
associated with atrophy and calcification of ipsilateral cerebral hemisphere
.It is caused by errors in ectodermal and mesodermal development. Manifests
with fits and hemiplegia on the opposite side
► Lymphadenopathy in young:
leukemia/lymphoma/disseminated tuberculosis
►Cyanosis –suggests Fallot’s
►Clubbing – TB, infective
endocarditis, bronchiectasis
▲Shortening of hemiplegic limb –
indicates it is dating from early childhood
►Irregular pulse of atrial
fibrillation.
BP must be
recorded always
IIIB. HIGHER
FUNCTIONS
A. Consciousness
B. Orientation
C. memory
D. intelligence
E. speech
F Emotion
G. judgment
H. behavior
I. Presence of hallucination
/delusion /illusion.
Levels of altered sensorium:
1.
Drowsy 2. Stuporous- Not easily arousable 3. Semiconscious-responding to painful
stimuli only. 4. Unconscius-No
response to even painful stimuli.
Condition with hemiplegia and altered level of consciousness
1. Cerebral hemorrhage
2. Extensive cerebral infarct
3. Raised ICT due to cerebral
edema
4. Infarct turning hemorrhagic
5. Meningitis or encephalitis
6. Brainstem lesions
7. Infra tentorial herniation
8. Trauma
9. Space occupying lesion:
tuberculoma or cerebral abscess
HANDEDNESS
The
hemisphere in which speech area is located is referred to as dominant
hemisphere
In
majority of right handed persons dominant hemisphere is on left side and vice
versa.
Damage
to speech areas in dominant hemisphere causes aphasia
In a right handed person damage
to left hemisphere can cause hemiplegia with aphasia
In 95% of right handed
individuals -left dominance occurs with speech area on left
In 70% of left handed –right
dominance
Types :of aphasia:
Broca’s aphasia (Synonyms: Motor
aphasia/Expressive aphasia/Non fluent Aphasia):
Inability to “express” though patient
understands what is being talked to.
ie. Verbal
comprehension is normal but unable to express.
Features affected: naming,
fluency, rhythm
Anomia;
Inability to name objects
Aggramatism:
disuse of connecting terms like “and”, ’the’ and ‘of’
Wernick’s aphasia (Sensory aphasia
/Receptive aphasia/Jargon aphasia)
Comprehension
and production of meaningful speech is affected.
Inability to understand spoken words in a
language well known to the patient.
Global aphasia: is a combination of
Broca’s and Wernick’s.
In
addition patient is unable to read or write. Comprehension is poor for spoken
words and written language.
Speech
areas
Located
in the dominant Hemisphere
Broca’s
Area: posterior 1/3rd of inferior frontal convolution-Area44
Wernick’s
Area: upper part of posterior temporal lobe and adjacent parietal lobe.
How to test for
aphasia:
Test for:
1. Fluency
2.
Naming
3.
Repetition
4.
Obeying of commands
5. Reading
6.
Writing
7.
Articulation
TECHNIQUE:
·
Engage
the patient in conversation and ask him to describe his illness.
·
Note
if speech is fluent or non fluent.
·
Does
the patient understand complex commands/simple commands?
·
Is
he able to read correctly?
·
Is
he able to write correctly?
·
Can
he name the objects?
·
Can
he recognize objects? if not – the condition is agnosia
·
Differentials for Aphasia:
Confusional states versus aphasia
Ask
patient his name, date and whereabouts; this will elicit
-an
inappropriate response if the patient is grossly aphasic
If
he is merely confused response will be appropriate but incorrect.
·
Akinetic
mutism:
Patient
lies apparently awake but is immobile and mute –with eyes open and fixing on
people or objects around the room.
The
site of lesion is in frontal lobe or in the region of 3rd ventricle
Dysarthria: poorly articulated speech;
muscles or nerves concerned in production of speech (peripheral apparatus of
speech) are dysfunctional in dysarthria
Dysphonia:
hoarse or whispered speech.
Orientation:
Orientation-in time, space, person are to be
tested
Organic
confusional state: Indicated by dementia and delirium
Dementia:
person is confused in time, place and person but he is alert and awake
Delirium:
patient is similarly confused but is having impaired alertness.
Delirium
occurs in alcoholism and atropine poisoning
Memory:
a. Immediate memory: memory lasting up to a minute or so.
Test:
Ask the patient to repeat 7digit number or 5 digit number
Ask
him to spell the word ‘world’ backwards or any short word
Ask
if he can remember telephone number while dialing
Give
an address to remember and ask to repeat after a short interval or distraction
or give 3 names to remember and recall after
2-5 minutes
Condition
where immediate memory is impaired: Korsakoff’s psychosis
.
b. Recent memory: Memory of events
which occurred in the last few days –events should be of personal importance or
world news
Check
with relatives or friends of the patient if he is correct.
c. Remote memory: is long term memory –is relatively resistant to loss
But
in progressive severe dementia, it can get lost.
Intelligence:
Affected
in dementia .To test –asks the patient to serially deduct 7 from 100 backwards
or add 7 forwards. (If the patient is literate)
Judgment:
Judgment:
Ask
him what he would do if fire breaks out or what he would do if an addressed
envelope is lying on the road.
Emotion:
Anxious
/depressed /elated /swings of moods.
IV. CRANIAL NERVES
Importance
of cranial nerve examination in
hemiplegia: (Table1)
Optic nerve - Papilledema in raised intracranial
tension
Tubercular
meningitis with hemiplegia can have optic
atrophy
Oculomotor nerve involved in Weber’s syndrome
(Fig1a)
Pinpoint
pupils in pontine hemorrhage
Abducens and facial
ipsilateral 6th
and 7th nerve palsy with contra lateral hemiplegia in Millard –
Gubler’s syndrome (fig1c.)
5th, 7th
and 8th Cerebellopontine
angle tumor with extension to cortico spinal tract
Pearls for practice
Important cranial
nerve signs to look for in hemiplegia
Papilledema (II)
Ptosis (III)
Abnormal/asymmetrical
pupils II, III)
Abnormal eye
position (III, IV, VI), conjugate deviation of eyes
Facial droop
Dysarthria
Learning points
1. UMN palsy of VII nerve lesion above Pons
2.
LMN palsy of VII nerve crossed hemiplegia
3.
Mimic
palsy- of frontal lobe lesion (emotional facial movements lost, voluntary
facial movements retained)
4.
Hemiplegia
without 7th cranial .nerve involvement is suggestive of lesion below
Pons
5.
Almost
all the cranial nerves receive bilateral innervations from the pyramidal tract.-
except CrNerveVII that innervates lower face.
Table.Cranial nerve syndrome associated with hemiplegia
   
V. SPINAL MOTOR SYSTEM
Points to note in the examination
of the spinal motor system: (chart3)
Hemiplegia often
Wasting of the muscles is a very
late phenomenon in UMN hemiplegia-
1. Nutrition:
- wasting occurs commonly in chronic
hemiplegia in small muscles of hand- due to
disuse
atrophy
2. Power:
Often groups of muscles are
involved-(UMN Lesion);
Often distal muscles are involved
·
Grading
of power
0.
absent movements
1.-flicker
of contraction
2.
Movements with gravity eliminated
3.
Movements against gravity, not against resistance
4.
Movement against gravity and resistance but less than normal
5.
Normal power
Law of dissolution;
Movements which are lost late in
evolution are first to be affected and last to recover-
e.g. Fine movements
3. Tone:
Tone is a state of partial
contraction of resting muscles which helps in maintenance of posture.
Spasticity: is Velocity dependant increase
of muscle tone in response to passive muscle stretch.
·
Spasticity is a sign of pyramidal lesion found
commonly in hemiplegia
·
Clasp-
knife type
of spasticity is typical.(resistance to passive movements with
sudden giving way, usually towards
completion of joint flexion or extension)
·
.
In upper limbs – tone is more in flexors than extensors (flexor predominance)
·
In
the lower limbs –extensor predominance
Thus tone is more in antigravity group of
muscles
Clonus: sustained clonus is a sign of
pyramidal tract lesion.
Clonus is a series of rhythmical
contraction occurring in response to maintenance of tension in muscle tendon
(in ‘pseudo clonus’ contractions are not sustained)
Clonus is due to gamma
neuron discharge.
Sites where elicitable:
Ankle
clonus: elicited by forcibly dorsiflexing the foot after flexing the hip and
knee
Patellar
clonus: by sharply moving the patella downwards.
Wrist
clonus: by suddenly and forcibly dorsiflexing the wrist.
Finger
clonus: by suddenly extending the fingers
Pseudo
clonus: is ill sustained; and is seen in tense individuals normally.
Flaccidity –in the initial state of
neuronal shock
Chart.3.Factors to be examined under spinal motor system 
Coordination: affected
if cerebellar lesion is associated
Involuntary movements: Accompany
if extra pyramidal lesion is associated.
Reflexes (table2)
For
convenience reflex examination is included after motor system
But
ideally must be tested after sensory system examination
DTR can
be reinforced by patient performing isometric contractions
(e.g.
clenching the teeth)
Deep tendon reflexes:
JAW JERK:
Relax
the jaw, open 1/3rd and keeping the thumb over the chin, tap the
thumb;
Response is closure of the jaw. Note the speed
of the closure
Exaggerated
jaw jerk occurs in pseudo bulbar palsy.
Pseudo
bulbar palsy may be associated with UMN lesion of the limbs.
Absent
jaw jerk or slight response is normal
Afferent:
V cranial nerve
Efferent: V cranial nerve motor
component
Biceps
Jerk: (Root
value C5C6) (Positioning-Elbow
flexed, forearm supinated)
Keep
the forearm supported on the patient’s thigh, or on examiner’s forearm.
Patient’s
forearm is held midway between flexion and extension.
Keeping
the thumb firmly over the biceps tendon and with fingers around the elbow,
-tap
the thumb briskly.
Normal
response is flexion of the elbow.
Lesion
above C5 causes exaggerated biceps reflex
Supinator
reflex: Root
value (C5C6) - (With elbow flexed, forearm pronated)
Strike
the radius 2cm above the wrist joint,
Response-flexion
of elbow and contraction of brachio radialis and flexion of fingers
Triceps
reflex; (root
value C7 C8)
Hold
the arm midway between flexion and extension, resting it on the thigh.
Tap
the triceps tendon just above the olecranon.
Normal response is extension of the elbow and
contraction of triceps.
Finger
flexion Reflex
(root value C7C8)
Blow upon the palmar surface of the
semi flexed fingers
Normal response-flexion of the
fingers and thumb.
Knee
Jerk ;( Root
valueL2, L3, L4)
Let
the knee swing free by the side of the bed with the patient sitting up.
Tap
the quadriceps tendon below the patella
Response:
Extension of the knee and contraction of the quadriceps.
Ankle
jerk (root value
L5S1)
Flex
the knee, rotate the thigh externally, slightly dorsiflex the foot and tap the
Achilles tendon.
Response:
plantar flexion of the foot and contraction of gastroconemius
Reinforcement of deep tendon reflexes;Ask the patient
to clench the teeth or for lower limb reflexes have the patient to hook
together their flexed fingers and pull apart-(Jendrassik maneuver)
Grading
of Reflexes:
Refer Chart 4.
Superficial reflexes in
hemiplegia:
Importance of abdominal reflex:
Abdominal
reflex and cremastric reflex loss-is
a sign of UMN lesion.
But loss is not dependent on the severity of
pyramidal lesion.
In congenital
diplegia and motor neuron disease –not lost till late.
But lost very
early in multiple sclerosis
.
Abdominal reflex
To elicit:
Stimulus is a scratch or stroke on anterior abdominal wall
Trace the scratch
from outwards to inwards
Look for
contraction of abdominal muscles and
Movement of
umbilicus towards stimulus
Contra lateral
side –contraction lost- in (a).pyramidal lesion
Same side –contraction lost-in (b) LMN lesion (T7 –T12)-in paraplegia
Root value for
abdominal reflex
Epigastric region –T7-T9
Upper abdomen --
T9-T11
Lower abdomen--
T11-T12
Superficial
abdominal reflex lost also in: obesity, elderly, muscle wasting, rigidity
Cremastric
reflex
Root value; L1
Test in lying or
standing posture
Stroke over inner upper
aspect of thigh from above downwards and inwards
Response: testes
moves upwards
Absent
in------------pyramidal tract lesion
LMN lesion at L1
Non pyramidal
lesion where cremastric reflex is lost/diminished – varicocele
In
hemiplegia-superficial reflexes affected are abdominal, cremastric, plantar.
In Lower Limb
Plantar reflex:
abnormal extensor plantar reflex is
positive babinski sign
·
Eliciting
plantar reflex:
o With the patient lying supine,
-‘flex the knee, fix the foot’
with ankle externally rotated
Using blunt object
Stroke on lateral aspect of foot
o Normal response:
Plantar flexion of great toe and
plantar flexion of other toes
·
Root
value: L5, S1
Types
of Babinski response: (chart 6)
·
True Babinski sign:
Extension of great toe with or
without
-fanning and abduction of other
toes;
Fully developed response involves
above response plus
-dorsiflexion of ankle plus
flexion of knee and hip with slight abduction of the thigh causing withdrawal
of leg.
,
·
Minimal Babinski:
No movements of the toes
Contraction of tensor facia lata and of
adductor muscles of thigh - can be only felt.
·
Equivocal
Babinski sign:
Initial flexor movement of the toe followed by extension.
Babinski
mimickers
Pseudo Babinski sign occurs-
a. If the short flexors of the
toe are paralyzed (Inverted plantar)
b. In athetosis or chorea when
the involuntary movement is super imposed at the time of eliciting the reflex,
the great toe may extend as a part of athetoid movement
c. In case of plantar
hyperesthesia,
-application of strong or painful
stimulus to the sole of the foot produces ‘withdrawal response’
Positive
bilateral
Babinski in absence of
pyramidal lesion:
Positive
bilateral
Babinski in absence of
pyramidal lesion:
a.
Infants
before age one b. deep sleep .c. deep anesthesia d.post
ictal state e. coma.
Other methods of eliciting plantar reflex:
(These methods test positive in extensive
pyramidal lesions)
§
Oppenheim’s
method: firm stroke applied down on either side of anterior border of
-tibia with finger and thumb.
2. Gorden reflex: the calf muscles
are squeezed.
3. Chaddock method: A curved
stroke applied below the lateral malleolus.
Absent Babinski response in the presence of
pyramidal lesion:
In S1 lesion with
paralysis of extensor hallucis longus.
Chart6.Types of Babinskis response
Gait
Gait in hemiplegia
:( circumduction gait)
Patient has
difficulty in flexing the hip, knee and ankle since flexor muscles are weak in
the lower limbs and tone is increased in the anti gravity muscles. Patient
therefore drags the foot.
The foot is raised
from the ground by tilting the pelvis and the leg is swung forward in
semicircle from the hip, so the foot tends to describe an arc, the little toe
scraping along the floor.
(Hip- is tilted
upwards and abducted.
Knee – stiff and
hyper extended
Ankle –excessively
plantar flexed and may invert (equino varus)
Upper arm adducted
and flexed with minimal swing of shoulder; elbow and wrist flexed
VI. Examination of sensory system
Hemi sensory loss
can occur in thalamic or cortical lesion along with hemiplegia
not common –hence details of exam of sensory
system –not dealt with in this article
VII.Cerebellar Examination
Abnormal signs in
hemiplegia are caused by medial medullary syndrome.
VIII.Extra pyramidal signs in hemiplegia
Occur in pseudo
bulbar palsy.
IX.Examination of other systems
Cardio
vascular System: look for signs
of congenital, valvular, and hypertensive heart diseases
Respiratory system: Look for-Tuberculosis, lung abscess,
bronchogenic carcinoma
Abdomen: Look for
hepatosplenomegaly, mass abdomen.
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