Stroke- History, Examination, Management, Discussion

Faculty wise points

• Dr. Hamide- Integrate the risk factors into the history
• Dr. Vivekanandan- Include DM and HTN in HOPI,

1. History

Demographic details

Dextrousness (not needed)- Right/Left handed-

How to determine? Roll a paper and ask the patient to look through it. If a person is right handed,
they will use their right eye and vice versa. Or ask the patient to kick a ball.
Significance? Right handed people mostly have left hemispheric dominance (language centre located
in left hemisphere) and vice versa.

Definitive test for hemispheric dominance- Wada test (Intracarotid Sodium Amobarbital Procedure
ISAP). A barbiturate, usually Sodium amobarbital, is injected into one carotid artery so that the
corresponding hemisphere is anaesthetised. Then the neurologist tests the function of the un-
anaesthetised hemisphere in language and memory.

Education status‐ for MMSE purpose- if a patient is illiterate, he won’t be able to go through MMSE.

Source of history: If not from the patient, state the source of history. Say “Reliability is fair”

Chief Complaint‐ Weakness in the R/L UL/LL/both for the last ___ days

HOPI:

Histories to be asked
• At onset- loss of consciousness, seizures, deviation of angle of mouth, speech difficulty
• Weakness- onset, progression, degree of weakness, tone, truncal and neck involvement
• Raised ICT features
• Sensory features
• Cranial nerve features
• Abnormal movements
• CVS
• Drug
• DM, HTN
Patient was apparently asymptomatic ___ days ago when he developed weakness in <limb>.
Classic history‐ embolic stroke- while doing normal work; thrombotic- on waking up from sleep;
haemorrhagic- after strenuous work

Points in motor history

• At the onset of weakness, was there loss of consciousness/seizure/speech deficit/deviation
of angle of mouth?
• Persistent vs intermittent
• Rigid/flaccid weakness
• Degree of weakness- paresis vs. plegia
• Static/dynamic weakness
• Proximal vs distal
 • Involving or sparing the trunk
• Diurnal variation
• Pyramidal vs extrapyramidal
• Pain
• Abnormal movements
• Bowel and bladder
Proximal vs. distal weakness?‐
• combing/squatting/standing (from sitting position) vs. buttoning shirt/mixing food/wearing
slippers (Note- try to ask at least two questions for each weakness)
• Myopathies typically present with proximal weakness. They have pseudohypertrophy (bulk
increased but power decreased). No sensory loss, normal reflexes, may have hypotonia and
are more often hereditary.
• Peripheral neuropathies typically present with distal weakness. They have sensory deficits (
glove and stocking), bilaterally symmetrical involvement, paraesthesisas and numbness.
Distal reflexes like ankle jerk are abolished. Tone is decreased in distal muscles and wasting
may be there.
• GBS is a neuropathy which presents with proximal muscle weakness
Neck involvement?
Breathing difficulty?

Progression‐

Feature Thrombus Embolus Haemorrhagic

Progress Can be maximal at • Maximal at
onset or progress over onset Sudden onset with
minutes to hours • Rapid progression over
improvement minutes to hours
may occur May be catastrophic
Features of raised ICT May develop later May develop later Develops early in
large bleed

• Classically embolic stroke will improve with time because the embolus gets lysed and
dissipates.
• Thrombotic stroke- 50% will be maximal FND at onset, and in the other 50%, the FND will
progress gradually
• If progressive, how much time did it take to progress from UL to LL? What was the patient
doing at the time? How was the work affected?
• Was the patient able to walk when transported to the hospital? How many people took the
patient? How (stretcher/wheelchair)?
• Intermittent weakness- electrolyte imbalance like hypokalaemic periodic paralysis.
• Remission-exacerbation pattern of weakness- MS
• Progressive motor weakness- malignancy
• Recovering motor weakness- infection
• Slowly progressive motor weakness- degeneration

Degree of weakness
• Hemiparesis- more likely cortical involvement
• Hemiplegia- more likely internal capsule
• Ask about walking, how much they can use the limb
Truncal weakness
• Can the patient get up from bed?
• Can the patient move around in bed?
• Truncal weakness suggests cerebellar involvement

h/o loss of consciousness? Large cortical lesions due to raised ICT. Brainstem lesions because the
reticular activating system is in the brain stem. (No loss of consciousness does not rule out lesions
here)

h/o seizures?- Cortical lesion. Arterial strokes rarely present with seizures because the neurons lose
blood supply, whereas in venous thrombosis, the neurons have arterial supply left so they can fire.
Note- Todd’s paralysis- transient weakness in a part of the body after a seizure. Resolves in 48 hours.
History in a seizure:
Biting of tongue
Loss of consciousness
Frothing at mouth

Character Vasovagal Syncope Seizure

Trigger Typically present- illness, pain, Often none, but can be sleep
emotion deprivation, alcohol, drugs
Prodrome Feeling faint, tinnitus, nausea, Not always present.
dimming of vision
Duration of unconsciousness <60 seconds 1-2 minutes
Convulsion May occur but brief myoclonic Usually 1-2 minutes in tonic
jerks clonic
Colour Pale/grey Red/blue, may be pale
Lateral tongue biting Very rare (may bite tip) Common
Recovery Rapid, no confusion Gradual, over 30 minutes,
often confused, amnesic.

Could the patient speak at the time?

Bowel and bladder dysfunction at the time and currently?

Rigid vs Flaccid weakness

• Rigid weakness- feels the limbs to be stiff- UMN
• Flaccid weakness- feels the limbs to be floppy- LMN type
• Stiffness can be due to Pyramidal or Extrapyramidal lesions. Extrapyramidal lesions however
will have only stiffness but no weakness.
h/o abnormal movements‐
• fasciculations are seen in LMN lesions
• If there are any other abnormal movements, consider extrapyramidal disease.
Sensory history‐
• loss of sensation of temperature while bathing.
• Loss of touch- can you feel your clothes on your body?
• Tingling/numbness?
• Can you feel the ground with your feet?
Pain
 • Pain and weakness can be seen in muscle disease. Polymyositis can have pain and weakness.
The weakness will be in proximal muscles.
• Radicular pain can be a harbinger of compressive myelopathy.
• Extramedullary compression has prominent radicular pain.

History suggestive of raised ICT: Headache, projectile vomiting, Transient visual obscuration (Dr.
Vivekanandan)

Autonomic history: esp bowel bladder. Bladder involvement is commonly seen in cord lesions.

Cranial nerves history‐ Quick comment “No h/s/o other cranial nerve involvement (if VII nerve is
involved)
I – alteration in smell
II – blurring of vision/diminished vision, differentiate colours, night blindness
III, IV, VI – drooping of eyelids/ double vision/ able to move eyes in all directions
V – having sensation over the face, able to chew food
VII – able to close the eyes and lips, deviation of angle of mouth, drooling of saliva, able to
feel taste of objects
VIII – hard of hearing, tinnitus, vertigo
IX, X – difficulty in speech, nasal twang to speech, nasal regurgitation, difficulty in
swallowing
XI – move the neck in all directions, lift the shoulder
XII – able to roll the tongue and push the food backwards

History suggestive of infection‐ TB meningitis, tuberculoma, TB vasculitis can be stroke mimics.

h/o evening rise of temperature, loss of wt, loss of appetite
h/o ear discharge- CSOM

CVS History‐ A fib. Ask all the cardinal symptoms- chest pain, dyspnoea, palpitations, syncope, pedal
oedema

Drug history
Look out for:
• Oral contraceptive pills
• Digoxin for A fib- a tablet which is given only 5 or 6 days in the week (to avoid toxicity)
• Warfarin- haemorrhagic stroke- tablet given in the evening because PT/INR is done in the
morning lol
Past history
• Past history of weakness- look out for any previous TIAs or strokes
*** Elicit the history points that were risk factors for the stroke (Dr. Hamide)

Summary (Sample)
An elderly diabetic and hypertensive man presented with sudden onset weakness of his right upper
limb and lower limb which gradually progressed and was associated with deviation of angle of
mouth to the left side. (Integrate the risk factors also)

Interpretation of history
 • Refer the table for thrombotic vs. embolic vs. haemorrhagic
• Stroke vs. stroke mimics
• Even in a hypertensive patient, thrombotic strokes are more common than haemorrhagic
stroke

EXAMINATION

General examination
PR- Irregularly irregular pulse in A.fib
BP- Cushing’s reflex, risk factor for stroke
RR- Irregular respiration in Cushing’s triad
Temperature
Pallor
Icterus
Cyanosis
Clubbing
Lymphadenopathy
Oedema

NEUROCUTANEOUS MARKERS
1. TUBEROUS SCLEROSIS – adenoma sebaceum, shagreen patches, ash leaf macules
2. NEUROFIBROMATOSIS – cafe au lait spots, neurofibromas, periungual fibromas,
axillary freckling
3. VON-HIPPEL LINDAU SYNDROME – conjunctival hemangioma
4. STURGE WEBER SYNDROME – port wine stain(capillary hemangioma)
5. ATAXIA TELANGIECTASIA – telangiectasias, especially on the conjunctiva
6. SPINA BIFIDA – tuft of hair
7. FRIEDREICH’S ATAXIA – pes cavus

General examination
• Pallor- B12 deficiency
• Icterus- Hepatic encephalopathy, Kernicterus
• Clubbing- IE
• Lymphadenopathy- Disseminated TB
Focussed general examination for stroke in the young
• Arcus juvenilus
o Arcus senilis starts superiorly and no iris is visible between limbus and arcus
o Arcus juvenilis starts inferiorly and iris is visible between limbus and arcus (Lucid
interval of Vogt)
• Xanthoma- larger, tumour like xanthelesma
• Xanthelesmata
• Frank’s sign- Earlobe creases
• Signs of rheumatic activity
• Signs of infective endocarditis
Neck Examination
Carotid bruit
Thyroid enlargement- may obliterate carotid pulse, may itself cause a bruit which can be mistaken
for carotid bruit
Neurological Examination

Follow this order:

• Higher mental function
• Cranial nerves
• Motor system (includes all of these components. Every one of them must be examined in a
motor system short case)
o Bulk
o Tone
o Power
o Superficial reflexes
o Deep tendon reflexes
o Coordination
o Gait and Stance
o Involuntary movements
• Sensory system
• Signs of meningeal irritation
Higher mental function: Comment- “Conscious, oriented to time, place, person. Memory, speech
are normal”
• Consciousness
• Orientation
• Memory
• Speech and language
• Apraxia – difficulty with motor planning to perform purposeful tasks, provided the
command is understood
• Agnosia- Inability to process sensory information
Motor System Examination
 Bulk
• Measure at some clearly defined point wrt a bony process
• Customary points to measure bulk
o 18cm above patella
o 10cm below tibial tuberosity
o 10cm above and below olecranon
Tone
• Tone is defined as the resistance offered to passive movement by a resting muscle
• Check tone at the shoulder, elbow, wrist, knee, hip, ankle joints
• Remember that to check tone in one muscle, you need to do its antagonistic
movement
• Say spasticity instead of increased tone (then get ready for all the questions on
spasticity, rigidity, paratonia etc)
• *****Causes of hypotonia (Dr. Hamide)
1. LMN type of paralysis
2. Spinal shock
3. Cerebellar lesions
4. Chorea

Power
MRC grading of power

Check power at all the joints

Comment on handgrip as percentage

1- No muscle contraction visible

2- Flicker of contraction, but no movement
3- Joint movement when effect of gravity is eliminated
4- Movement against gravity but not against resistance
5- Movement against resistance but weaker than normal
a. 4-:
b. 4
c. 4+
6- Normal power
Reflexes- If there is a low response, do Jendrassik’s manoeuvre if possible
If hyperreflexia is present, check for clonus in the ankles and knees

I. Superficial Reflexes
a. Corneal
b. Conjunctival
c. Abdominal (T8-T12)- MacLeod
d. Cremasteric (L1)- DO NOT MISS THIS IN A MALE PT
e. Plantar Response L5-S1

II. Deep Tendon Reflexes- Root values from MacLeod

• Ankle jerk- S1
• Knee jerk- L3, L4
• Triceps jerk- C7
• Supinator jerk- C6
• Biceps jerk- C5
Cranial Nerves Examination

1. Olfactory- Ask the patient to smell some known things like mint oil
2. Optic- Visual field by confrontation, Colour vision, Visual acuity
• Menace reflex- in patients who do not cooperate with confrontation. The patient is
asked to look straight ahead. A menacing stimulus like a hand is rapidly brought
towards the patient’s face from one side. Reflex blinking occurs.
3. Oculomotor, Trochlear, Abducens- H movement. Light reflex in III nerve‐ Dr. Hamide
• IIIN palsy- Pupil dilated, resting position of the eyeball is lateral deviation
• IVN palsy- the adducted eye does not move downwards (superior oblique
dysfunction)
• VIN palsy- the adducted eye doesn’t abduct fully
• Saccadic movements
• Pursuit movements
4. Trigeminal- Sensory: Forehead, upper part of the sides of the nose, upper lip, chin. Motor-
Ask the patient to clench their teeth and palpate temporalis, palpate masseter. Ask the
patient to open their jaw against resistance. Jaw jerk and corneal reflex.
5. Facial Nerve-
• Ask the patient to wrinkle their forehead by looking upwards
• Ask the patient to close their eyes tightly. Resist attempts to open them.
• Look for Bells phenomenon
• Say “eeee”
• Inflate their mouth with air.
6. Vestibulocochlear nerve-
• Rinne- 512 Hz tuning fork on the mastoid process. Ask the patient if they can hear it.
Once they can no longer hear it, move the tuning fork to the EAM
• Weber
• Why 512 Hz?
• Falls in mid-speech frequency range
• Lesser overtones
• Lower frequencies produce more vibratory effect
• Optimal tone decay time- higher frequencies have faster decay time
7. Glossopharyngeal, Vagus- Symmetry of palatal arches and pharynx, Gag reflex
• Gag reflex- use a tongue depressor to depress the tongue. Using a swab, touch the
palate or the pharynx on one side. Note the contraction of the palate, pharynx and
posterior 1/3 of the tongue (Sethuraman)
8. Spinal Accessory Nerve- elevate the shoulder against resistance, Turn face to one side
against resistance. Inspect and palpate the opposite SCM. Trapezius- shrug shoulders
against resistance
9. Hypoglossal- Protrude the tongue, lick teeth

Sensory Examination
• Fine Touch- Ask the patient to look away /close his eyes. Use cotton wool and dab.
• Crude Touch-
• Pain- Use a neurological pin
• Vibration- 128 Hz tuning fork. Put it over bony prominences (big toe and ankle- MacLeod)
Touch the fork to stop vibration to see for malingering. If sensation is impaired, keep going
proximally to the IP joint, medial malleolus, tibial tuberosity. Do the same for the upper limb
.
o Why 128 Hz for vibration? Lower frequencies tend to produce more vibratory effect
and tend to decay slower?
 • Proprioception
(a) Position sense- Ask the patient to close his eyes. Then, set the given joint in a
particular position in space. Ask the patient to place the same joint of the other
limb in a similar position. If the other limb is paralysed, ask him to repeat the
same action with the joint or ask him to describe the present spatial orientation
of the joint.
(b) Joint sense- Grasp the proximal interphalangeal joint of the great toe with the
thumb and index finger and then use the other hand to move the toe in
different directions (Ref Macleod P.269, Fig 11.31)
Cortical sensation examination- do it only if sensory examination is normal

• Stereognosis and Graphaesthesia- Ask the patient to close his eyes. Place a familiar object
like a coin or key and ask him to identify it (stereognosis). Use the blunt end of a pencil and
trace letters or digits on the patient’s palm and ask them to identify it (graphaesthesia)

Stance and Gait

• Stance- ask the patient to stand with his feet close together and eyes open. Swaying,
lurching or inability to stand with the feet together when the eyes are open suggests
cerebellar ataxia. Ask the patient to close his eyes but be ready to catch them. Repeatedly
falling is positive Romberg sign.
• Gait- Time the patient walking a measured 10 metres, turning through 180° and returning.
Note stride length, arm swing, steadiness, limping. Ask the patient to walk on the tip toes
then on the heels. Ask the patient to walk heel to toe in a straight line to test for gait ataxia.

Notes:
Higher mental function anomalies
• Consciousness
o Causes of coma-
▪ Trauma- cerebral contusion, concussion, subdural haematoma, extradural
haematoma
▪ Cerebrovascular disease
▪ Infections- meningitis, encephalitis, cerebral malaria
▪ Endocrine and metabolic disturbances- DM, myxoedema, uraemia,
Hypo/hypercalcaemia
▪

Hypertonia‐ there are three extremes. Note- antigravity muscles are flexors of the arms and
extensors of the legs
Feature Spasticity Rigidity
Seen in Pyramidal disease Extrapyramidal disease
Velocity Dependent Independent
More in Anti gravity muscles Equal in both
Phenomenon associated Clasp knife spasticity Lead pipe rigidity, Cogwheel
rigidity

• Spasticity: The hypertonia of pyramidal tract disease. Velocity dependent. When it reaches
considerable tension, there is a protective relaxation and a sudden ‘clasp knife’ loss of tone,
usually towards completion of joint flexion/extension. More in anti-gravity muscles.
• Rigidity: The hypertonia of extrapyramidal disease. Occurs throughout the range of motion.
No clasp knife phenomenon. Velocity and direction independent. Equal in flexors and
 extensors.
• Paratonia: Inability to relax muscles during muscle tone assessment. Feature of frontal lobe
disease. There are two types- oppositional and facilitatory
o Oppositional (gegenhalten)- when subjects involuntarily resist passive movements
o Facilitatory (mighalten)- subjects involuntarily assist passive movements
Examples of hypertonia
1. Clasp knife: feature of spasticity
2. Lead pipe: steady resistance throughout the range of motion. Feature of rigidity.
3. Cogwheel: Feature of rigidity. The affected limb gives in intermittently to the pulling of the
examiner. Seen in Parkinsonism.
4. Gegenhalten: (German- ‘against-stop’) Patient is unable to relax a group of muscles either
on request or passive stretching and actively appears to resist the movement. May indicate
that connections from the basal ganglia to the frontal lobe are impaired.
Testing power‐

Movement and joint Muscle Involved Nerve Supply Root Value

Shoulder abduction Deltoid Axillary nerve C5
Elbow flexion Biceps brachii Musculocutaneous C5,C6
nerve
Elbow extension Triceps brachii Radial nerve (C6),C7,(C8)
Wrist extension Flexor carpi ulnaris Radial nerve (C6), C7, (C8)
Flexor carpi radialis
Finger extension Extensor digitorum Posterior interosseous C7, (C8)
nerve, branch of
Radial
Finger flexion FDS, FDP Median, ulnar C8
Finger abduction First dorsal Ulnar nerve T1
interosseous
Finger adduction Second palmar Ulnar nerve T1
interosseous
Thumb abduction Abductor pollicis Median nerve T1
brevis
Hip flexion Iliopsoas Lumbosacral plexus L1, L2
Hip extension Gluteus maximus Inferior gluteal nerve L5, S1
Knee extension Quadriceps femoris Femoral nerve L3, L4
Knee flexion Hamstrings Sciatic nerve L5, S1
Foot dorsiflexion Tibialis anterior Deep peroneal nerve L4, L5
Foot plantarflexion Gastrocnemius Posterior tibial nerve S1
Big toe extension Extensor hallucis Deep peroneal nerve L5
longus
Extension of the toes Extensor digitorum Deep peroneal nerve L5, S1
brevis
Intrinsic muscles of the hand and their testing***
• Muscles of the thenar eminence- Median nerve
o Abductor pollicis brevis
o Flexor pollicis brevis
o Opponens pollicis
• Adductor pollicis- Ulnar nerve
• Hypothenar muscles
o Palmaris brevis- superficial branch of ulnar nerve
o Abductor digiti minimi- deep branch of ulnar
o Flexor digiti minimi- deep branch of ulnar
o Opponens digiti minimi- deep branch of ulnar
• Four lumbricals- lateral two by median nerve and medial two by ulnar nerve- Flex MCP and
extend IP
• Four palmar interossei- PAD- Palmar interossei adduct- deep branch of ulnar nerve
• Four dorsal interoosei- DAB- Dorsal interossei abduct- deep branch of ulnar nerve
Testing
• Pen test for Abductor pollicis brevis- Lay the hand flat on the table with the palm directed
upwards. The patient is unable to touch the pen held in front of the palm with his thumb
• Testing for opponens pollicis- ask the patient to touch the proximal phalanx of 2nd to 5th
digits with the tip of the thumb
• Card test- For Palmar interossei. Place a card between two of the fingers and try and pull it
out with your two fingers
o This can be modified to test for Adductor pollicis by placing the card between the
thumb and the index finger
• Book test/Froment sign- Adductor pollicis- Grasp a book between the thumb and other
fingers. The terminal phalanx of the thumb on the paralysed side becomes flexed at the IP
joint by FPL which is supplied by median nerve
• Lumbricals- flex at MCP against resistance.
Clonus
• Sudden stretching of hypertonic muscles produces reflex contraction. If this stretch is
maintained during the relaxation, then further reflex contraction occurs.
• Ankle clonus- flex the hip and the knee. Provide support under the knee but not at the calf.
Dorsiflex and evert the ankle.
• Sustained clonus: ≥6 downward beats of the foot.
• Ill sustained clonus: <6 downward beats of the foot.
• True clonus is the clonus associated with extensor plantar response
• Pseudoclonus: True clonus ceases with flexion of the great toe. Seen in anxiety,
thyrotoxicosis
Myotonia- delayed relaxation of a skeletal muscle following its contraction
Causes- myotonic dystrophy

Coordination
• Finger-nose test
• Finger-finger nose test: Patient should touch the examiner’s finger before touching their
nose. Can detect milder degrees of incoordination
• Heel to shin test detects lower limb incoordination
• Dysdiadochokinesis
• Other signs of cerebellar disease- nystagmus, ataxia, dysarthria, pendular reflexes,
hypotonia
Speech anomalies
• Definitions
o Dysarthria- Difficulty in articulating speech due to a motor deficit
o Dysphonia- loss of volume caused by laryngeal disorders
o Dysphasia- Abnormalities in speech production and/or understanding. It may also
involve other language symptoms like reading/writing unlike the previous two.
• Aphasias
o Broca’s aphasia- motor/expressive aphasia
o Wernicke’s aphasia- sensory/receptive aphasia
o Nominal aphasia- anomic aphasia

• Pathway of transmission
o The speech areas are located in the dominant hemisphere
o Sounds are recognised as language in the Wernicke’s area (area 22)
which is connected to a concept area where the meaning of the words is
understood
o The concept area is connected to Broca’s area (area 44,45), where
speech output is generated
o Wernicke’s area also is connected to Broca’s area directly by the arcuate
fasciculus.
• Wernicke’s aphasia (1)- Poor comprehension. Fluent but often meaningless
speech (as it cannot be internally checked). No repetition
• Broca’s aphasia (2) - Preserved comprehension. Non-fluent speech. No
repetition.
• Conductive aphasia (3)- Loss of repetition with preserved comprehension and
output
• Transcortical sensory aphasia (4)- Poor comprehension, fluent but meaningless
speech but intact repetition
• Transcortical motor aphasia (5)- Preserved comprehension, non-fluent speech
but repetition intact.
 • Dysphonia
o Disturbance of voice production
o May reflect vocal cord pathology like laryngitis or vagal anomalies
• Dysarthria
o With abnormal rhythm of speech
▪ Spastic dysarthria- Slurred, slowed and laboured. The patient barely opens
his mouth. Causes- pseudobulbar palsy, motor neurone disease
▪ Extrapyramidal dysarthria- monotonous, without rhythm, sentences
suddenly start and stop. Causes- Parkinsonism
▪ Cerebellar dysarthria- Slurred speech as if drunk. Sometimes canning speech
. Causes- Alcohol intoxication, MS, Cerebellar lesions
o With normal rhythm
▪ LMN
• Palatal- X nerve
• Tongue- XII nerve
• Facial- VII nerve
▪ Myasthenic
• Muscle fatiguability
Involuntary movements
•
Localisation

Hemiplegia ± VII N involvement

• Same side- Cortex/corona/capsule
• Opposite side (hemiplegia)- brain stem, spinal cord (C1-C4)
Cortex
• Not dense
• Hemiparesis/Monoparesis
• Seizure/altered sensorium
• Lobar dysfunction-
 o Dominant temporal- aphasia
o Non dominant parietal- hemineglect
• Cortical sensations lost- Two point discrimination, tactile localisation, graphaesthesia,
stereognosis

Subcortical
• Same as cortical but the cortical sensations are preserved
Internal capsule
• Dense hemiplegia (Power equally reduced to a marked extent UL and LL. Ex: UL and LL
power is 0/5)
• Hemianaesthesia
• Homonymous hemianopia
• Dysarthia
• Global aphasia (L side)
• Apractognosia
Abnormalities in Reflexes
• Main difference between superficial and deep reflexes
o Deep reflexes are monosynaptic- they go from the Ia afferent fibres in the muscle
spindle which synapse directly onto the α motor neurons of the spinal cord
o Superficial reflexes are polysynaptic- The sensory input needs to be processed at the
cortex before a response is elicited
Superficial reflexes

Abdominal reflex
• Absent abdominal reflex
o Pyramidal tract lesions above the level of T8
o Breech of the reflex arc due to Herpes Zoster, scars due to surgery etc
***Plantar response‐ L5, S1 (Sethuraman) but S1, S2 in MacLeod

Normal plantar response

• Flexion of the great toe and other toes
• Dorsiflexion at the ankle
• Flexion of knee, hip joints
• Contraction of tensor fascia lata
Extensor plantar response- the complete response is called Brissaud’s reflex
• Extension at great toe
• Fanning of other toes
• Dorsiflexion of ankle
• Flexion of knee, hip
• Contraction of adductor magnus (Dr. Hamide)
• Contraction of tensor fascia lata causing internal rotation of the hip
Standard reporting- choose any one
• Flexor plantar response
• Extensor plantar response
• Equivocal plantar response
• Mute plantar response
• Withdrawal plantar response
Minimal plantar response‐ On eliciting the plantar reflex, if there is no movement of toes, then
plantar response positivity can be assessed by feeling for contraction of tensor fascia lata and
adductor magnus.

Equivocal Babinski‐ Said to be equivocal in the following situations

• Rapid but brief extension of toes at first, followed by flexion or reverse.
• Only extension of great toe or extension of great toe with flexion of small toes.
• No response to plantar stimulation
• Flexion of knee and hip with no movement of toes
Pseudo‐ Babinski-
• Withdrawal response- eliminated by putting pressure on the great toe
• Chorea or athetosis
• If the flexors of the toe are paralysed in LMN

Conditions where Babinski is seen

• Infancy (up to 1 year of age)
• Deep sleep
• Deep anaesthesia
• Narcotic overdose
• Alcohol intoxication
• Coma
• Post ictal state
Other methods of eliciting Plantar response
• Oppenheim- Firm stroke with the finger and thumb down the anterior border of the tibia
• Chaddock- Light stroke from just below the lateral malleolus down to the small toe.
• Gordon- Squeezing of the calf muscle
• Schaefer- Deep pressure on achilles tendon
• Strümpell's- Forceful pressure over the anterior tibial region.

Physiology behind it
• Seen in infants up to 1 year. After that, the corticospinal tract becomes completely
myelinated and there is descending control over the reflex, so it switches to flexor response
to assist in ambulation.
• Why do we start from lateral side? Because, in initial pyramidal tract lesions, the receptive
focus is confined to the lateral aspect of the sole. As the lesion progresses, it can be elicited
from other parts also
• Why don’t we touch the ball of the great toe? If it is stimulated, the grasp reflex of the legs
may be stimulated causing flexion of the great toe even in the presence of a pyramidal tract
lesion
Upper limb equivalents of Babinski***
• Hoffman reflex- terminal phalanx of the patient’s middle finger is flicked downwards
between the examiner’s finger and thumb. In hypertonia, the tips of the other fingers flex
and the thumb flexes and adducts
• Wartenberg sign- Patient supinates his hand, slightly flexes his fingers with the thumb in
adduction. The examiner pronates his hand and links his flexed fingers with that of the
patient’s fingers. Both flex their fingers against each other’s resistance. In hypertonia, the
thumb adducts and flexes strongly. While normally, the thumb extends
Other superficial reflexes
• Cremasteric
o Stroke from below upwards
o Can also be done by giving a stroke at the level of the lower third of the adductor
canal
• Abdominal
o Absent abdominal reflex causes
▪ LMN at the level of the reflex arc
▪ UMN above the level of the reflex arc
• This is because the abdominal reflex also has a cortical pathway
apart from the spinal reflex arc
▪ Obesity
 ▪ Multiparous females
▪ Distended abdomen
Cranial nerve lesions

Olfactory nerve
• Abnormal finding- anosmia. Check if it is limited to one nostril or both
• Anosmia in both nostrils
o Common cause- common cold
o Hyposmia can be a feature of Parkinson’s
• Unilateral anosmia
o Blocked nostril
o Unilateral frontal lobe lesion like a meningioma or glioma- very very rare
Optic nerve
• Visual pathway and visual field defects
o The left temporal hemiretina captures images from the left nasal field and the right
nasal hemiretina captures images from the right temporal field. The right nasal
hemiretina crosses over.
o The left nasal hemiretina captures images from the left temporal field and the right
temporal hemiretina captures images from the right nasal field. The left nasal
hemiretina crosses over.
o From this, the optic tract is formed.
o The optic tract sends fibres to the lateral geniculate nucleus in the thalamus.
o From the thalamus, there are two projections to the visual cortex (called the optic
radiation)
▪ Meyer’s loop through the temporal lobe to the occipital lobe
▪ Baum’s loop through the parietal lobe to the occipital lobe
o Lesions and their effects
▪ Optic nerve (B)- The fibres capturing images from one eye are affected, so
total blindness of the ipsilateral eye
• Cause of lesion-
▪ Optic chiasm (C)- Since only the fibres of the nasal hemiretinas cross, there
is bitemporal heminanopsia
• Causes
▪ Optic tract (D )- The fibres of the contralateral nasal hemiretina and
ipsilateral temporal hemiretina. This is called homonymous hemianopsia.
• Causes-
▪ Optic radiation
• Meyer’s loop through the temporal lobe- Contralateral superior
quandrantanopsia (Pie in the sky defect)
• Baum’s loop through the parietal lobe- Contralateral inferior
quadrantanopsia (Pie on the floor defect)
▪ Occipital lobe lesions
• Commonly due to posterior cerebral artery strokes.
• However, the macula has a dual blood supply from the MCA as well.
• Hence there is macular sparing.
Oculomotor, Trochlear, Abducent lesions
• Extraocular muscles and their movements

• Superior rectus- Elevation, intorsion, adduction

• Inferior rectus- Depression, extorsion, adduction
• Superior oblique- Intorsion, abduction, depression
• Inferior oblique- Extorsion, elevation, abduction
• Lateral rectus- Abduction
• Medial rectus- Adduction
• SIN- Superiors intort
• Innervation
o SO4- Superior oblique by IV nerve
 o LR6- Lateral rectus by VI nerve
o Rest by III nerve
• III nerve palsy
o Features-
▪ Ptosis (due to paralysis of LPS)
▪ Deviation of eyeball- eyeball is turned down and out due to the action of SO,
LR
▪ Pupil is fixed and dilated due to paralysis of sphincter pupillae
▪ Accommodation is lost due to paralysis of the ciliary muscle
o Causes
▪ Pupil sparing III nerve palsy- the pupil is not dilated. Seen in Diabetes
mellitus, Hypertension, Collagen vascular disease, Atherosclerosis because
the parasympathetic fibres that supply the sphincter pupillae run outside of
the nerve. The vasa vasorum that are vulnerable to ischaemia do not supply
the sphincter pupillae.
▪ III nerve palsy affecting the pupil
• Aneurysms- Posterior communicating artery, Posterior cerebral
artery
• Uncal herniation
• Cavernous sinus thrombosis
▪ Unilateral ptosis- Horner’s syndrome plus the above causes
▪ Senile ptosis
▪ Bilateral ptosis
• Myasthenia gravis
• Snake bite
• Botulism
• Bilateral Horner’s syndrome
• Conjugate gaze and gaze palsies
• In this diagram, the person wants to look to the right. So the right eye is being ABducted (
Lateral rectus, VI Nerve) and the left eye is being ADducted (Medial rectus, III nerve)
• To look to the right, the signal arises from the left cortex from the frontal eye fields (area 8)
• From the FEF, the fibres cross the midline and reach the contralateral PPRF.
• From the PPRF, the fibres go to the abducent nucleus and reach the right lateral rectus
muscle.
• To reach the left medial rectus muscle, they go to the oculomotor nucleus by crossing the
midline and reaching the MLF.
• Lesions, their causes and their effects
o Left FEF- Both eyes can’t look right. So they slowly drift to the left
▪ Cause- frontal lobe seizures/frontal lobe lesions
o Right PPRF or Right VI nucleus (both have the same effect because they are so close
). Both eyes can’t look right (lateral gaze palsy)
▪ Cause- medial pons lesions
o Left MLF- left eye can’t look right (affected eye cannot adduct) while right eye can
look right (unaffected eye can abduct)- this is called Internuclear ophthalmoplegia.
Convergence is intact (mediated by another pathway) and the unaffected eye
 develops nystagmus
▪ Commonly occurs in multiple sclerosis because the MLF is highly myelinated
o One and a half syndrome
▪ Damage to the PPRF+MLF
▪ INO plus loss of lateral gaze to the affected side.

• Pupillary lesions and ptosis- more details in the spotters document

o Light reflex pathway
▪ Optic nerve, optic chiasma, optic tract, Pretectal nucleus, bilateral Edinger
Westphal nucleus, oculomotor nerve, ciliary ganglion, short ciliary nerves,
sphincter pupillae, bilateral pupillary constriction
• Abnormal pupils

Trigeminal nerve
• Three nuclei of the trigeminal nerve
o Principal sensory nucleus- dorsal column sensations to the face
o Mesencephalic nucleus- proprioception of the muscles of mastication and the
periodontal membrane. Prevents one from biting too hard.
o Spinal nucleus- crude touch, pain, temperature from the ipsilateral face. It goes as
low as C2 before it crosses and ascends in the medial lemniscus
• Muscles of mastication- all are supplied by the mandibular nerve (V3)
o Masseter- elevation of the mandible
o Temporalis- Elevation of mandible
o Medial pterygoid- elevation of mandible
o Lateral pterygoid- depression of the mandible
• V nerve motor weakness- jaw deviates towards the affected side
• Jaw jerk- afferent and efferent is V nerve
• Corneal reflex- afferent is V and efferent is VII
• Cause of V nerve lesions
o Nuclear lesions- pons, medulla, upper cervical cord (which is why V nerve should be
examined carefully in quadriplegia)
▪ Tumour, demyelination, vascular lesions, syringomyelia
o Preganglionic lesions- Tumours (meningioma, CP angle tumour), meningeal irritation
. Usually accompanied by other CN palsies like VI, VII, VIII
o Gasserian ganglion lesions
 ▪ Tumours, abscess, Herpes zoster ophthalmicus (ophthalmic division of V
nerve)
▪ Raeder’s paratrigeminal syndrome- lesions close to the Gasserian ganglion.
Unilateral Horner’s without facial anhidrosis (because the sudomotor fibres
to the face are not involved) and ipsilateral loss of facial sensation
o Postganglionic
▪ Cavernous sinus
▪ Gradenigo syndrome- petrous part of temporal bone
▪ Superior orbital fissure syndrome
Facial nerve
• LMN facial palsy
o Mouth deviates to normal side
o Loss of nasolabial fold on affected side
o Bell’s phenomenon- as the patient tries to close his eye, the eyeball rolls upwards,
exposing the conjunctiva below the cornea
o Loss of frontal wrinkling on affected side
• UMN facial palsy
o Mouth deviates to normal side
o Loss of nasolabial fold
o No Bell’s phenomenon
o Frontal wrinkling intact
• For more info, refer the spotters document
• Remember, in Right sided hemiplegia, the lesion is RIGHT UMN FACIAL PALSY which
causes deviation of angle of mouth to the left
Test Muscle being tested Inference
Wrinkle forehead Occipitofrontalis Absent on affected side in
LMN facial palsy
Close the eyes tightly and Orbicularis oculi Examiner can open the eyelids
attempt to resist opening by easily in LMN
examiner
Smile showing teeth (EEEEEE) Levator anguli oris Deviation of angle of mouth
Puff cheeks Buccinator Can easily be unpuffed in LMN
or UMN
Clench teeth and make a face Platysma Normally longitudinal folds of
skin are visible in the neck

Glossopharyngeal and vagus

• In unilateral conditions, the ipsilateral palatal arch is at a lower level than on the healthy side
o Note- uvula deviates away from the affected side, but never give this as justification
for X nerve palsy because the position of uvula is variable even in healthy individuals
. Senior examiners expect palatal arches to be reported.
• Palatal myoclonus- Autosomal dominant cerebellar ataxia (ADCA)
• Exaggerated gag reflex- pseudobulbar palsy
• How to distinguish between pure IX and pure X palsies?
o Alagappan- In pure X nerve palsy, the patient is able to feel the tickling sensation of
the throat but there is no contraction in the gag reflex
Spinal Accessory nerve
• Unilateral SCM paralysis causes weakness in movement to the opposite side
• XI nerve palsy- Jugular foramen syndrome (IX, X, XI), Lateral medullary syndrome
Hypoglossal nerve
 • UMN palsy of tongue- no true wasting, no fibrillation, protrusion of tongue is difficult,
tongue is small and spastic
o Jaw jerk exaggerated bilaterally- sign of pseudobulbar palsy
• LMN tongue- wasting, fibrillation, tongue can be protruded and is deviated to the affected
side, flaccid tongue

Sensory deficits
• Pathways- refer the discussion part of the document
• Exteroceptive sensations- those which are derived from sources outside the body. Include
pain, temperature and fine touch
• Proprioceptive sensations- Position, vibration, deep pain. Derived from impulses from the
body itself
• Romberg’s test
o Ask the subject to stand erect with the feet together and eyes closed. Positive sign is
noted when a swaying or toppling occurs. Called Romberg’s positive
o Inference- Balance is maintained by vestibular function, proprioception and vision.
When vision is taken away, the other two have to maintain. If there is a lesion in
either of the two pathways then Romberg’s is positive
o So, Romberg’s positive means either defective proprioception or defective vestibular
function.
• Cortical sensations
o Function of sensory cortex- Accurate localisation of stimuli and assessment of shape,
weight, texture of objects
o Tactile localisation- Localises accurately where the patient was touched
o Two point discrimination- 2-3 cm on the palm
o Stereognosis- recognition of an object purely from the feel of its shape and size
o Graphaesthesia- Ability to recognise numbers/letters/diagrams written on the skin
with a blunt point
Cerebellum
• Cerebellar nuclei
o Dentate nucleus- contralateral VA/VL nuclei of thalamus
o Emboliform and globose nuclei- contralateral red nucleus
o Fastigial nucleus- vestibular nuclei and reticular formation
• In general, the cerebellum controls the ipsilateral half of the body because the cerebellar
input reaches the contralateral cortex which goes to the contralateral half of the body
• Lateral lesions of the cerebellum
o Affect the extremities- distal parts
▪ Can’t do finger-nose test
▪ Intention tremor
▪ Fall towards injured side
o Involve the hemispheres and dentate nucleus
• Midline lesions of cerebellum
o Affect the trunk
▪ Truncal ataxia
▪ Can’t stand independently
▪ Fall over when sititng
o Involve the vermis, emboliform, globose, fastigial nuclei
o Flocculonodular lobe also- nystagmus, vertigo
• Cerebellar ataxia
o All cerebellar lesions
o Loss of balance
 o Wide based gait- will fall if the feet are together
• Hypotonia
• Scanning speech
• Dyssynergia- dysmetria (finger-nose), intention tremor, dysdiadochokinesia
• Nystagmus- vertical
• Nausea, vomiting, vertigo

Gait and Stance

• Abnormal gaits
o Hemiplegic gait/Pyramidal gait/Circumduction gait- Components
▪ Adduction at shoulder
▪ Flexion at elbow, flexion at wrist
▪ Hand pronated
▪ LL extended at hip and knee
▪ Ankle and toes are plantar flexed
▪ Toes strike the ground while walking. To prevent this, the gait is of
circumduction type.
o Festinant gait of Parkinsonism- short, shuffling steps
o High stepping gait of foot drop
o Waddling gait of myopathy
o Ataxic gait of cerebellar disease
o March e petit pas
Abnormal movements
• Chorea***- Non/quasi purposive, non-repetitive, jerky, irregular, dance like movements
o Causes of chorea- Syndenham’s chorea (St. Vitus’ Dance), Huntington’s chorea, SLE,
Wilson’s, Chorea gravidarum (post rheumatic recurrence of chorea in pregnancy),
Hyperthyroidism
 • Tremor
• Athetosis
• Ballismus
• Myoclonus- Rapid, irregular, jerky movements that persist even during sleep
• Dystonia
• Dyskinesia
• Tics- Rapid, repetitive, coordinated, stereotyped movements that can be mimicked

Discussion

***Definitions

1. Stroke‐ A sudden and dramatic onset of focal neurological deficit from a vascular aetiology.
(Dr. Vivekanandan). The main deficit occurs over several hours, but not beyond 12 hours and
persists for more than 24 hours.
2. TIA‐ Sudden onset of focal neurological deficit from a vascular aetiology where the patient
recovers completely within 24 hours.
Most TIA last for 5-20 minutes. Episodes that last for >1hr are generally due to small infarcts.
Once there is an infarct, there is no more TIA concept.
80% affect anterior circulation, 20% affect posterior circulation
3. RIND (Reversible ischaemic neurological deficit)- Neurological deficit lasting more than 24
hours, but less than 7 days. (<3 weeks- Alagappan)

Classification (Ref- Davidson’s)

Management of Stroke

Investigations

Airway‐ Aspiration is common

Breathing‐
• Decreased cerebral perfusion
• Medullary injury dysregulated breathing

Circulation
• Bradycardia suggests raised ICT which may be due to haemorrhagic stroke. CT scan
rules out haemorrhage.
• Recommended antihypertensives: Labetalol, Nitroglycerine, Hydralazine,
Nicardipine, Clevidipine
• BP targets: (In ischaemic stroke, cerebral perfusion pressure has to be maintained,
so BP targets are a bit higher. (umbra penumbra concept- read) But in haemorrhagic
stroke, more bleeding can happen so BP has to be brought down much lower.)
o Haemorrhagic stroke- BP should be aggressively brought down. Target <140‐
160/90 mmHg.
o Ischaemic stroke
▪ If considering rtPA, BP should be <185/110 mmHg
▪ If not considering rtPA or it isn’t available, BP should be <220/120
mmHg(Sometimes the examiner will not accept 220/120. If they
don’t accept it, then say 180/120. There are two guidelines, which
 say the target BP should differ depending on the availability of ICU
facilities). Don’t give antihypertensives in this case unless there is
hypertensive emergency.
NCCT changes s/o infarct
• Loss of grey-white differentiation
• Loss of gyri-sulci differentiation
• Midline shift
• Ventricular compression
• Insular ribbon sign???

Thrombolysis‐ TENECTEPLASE in JIPMER

Indications (ABCDE)
▪ Clinical diagnosis of stroke
▪ <4.5 hours before first onset of symptoms
▪ Age >18 years
▪ CT scan excludes haemorrhage (Oedema >1/3 of MCA territory- ischaemia cannot be
visualised this early)

If the stroke is thrombotic and resolvable, physiological mechanisms would have already taken place

Contraindications
▪ BP >185/110 mmHg
▪ Bleeding propensity- Thrombocytopaenia, raised PT-INR, Heparin
▪ Previously thrombolysed in the past 24 hours
▪ Rapid improvement
▪ Recent MI- PT INR has to be maintained at a higher level.
▪ Coma
Note: Aspirin use is not a C/I for thrombolysis.

Method
▪ 2 peripheral iv lines
▪ 0.9 mg/kg rtPA, maximum 90 mg.
▪ 10% bolus dose.
▪ Remaining 90% over 1 hour.
▪ Treat arrhythmias, if any
▪ Give inotropes if BP is low.
▪ NG tube if required.
▪ If there is a high risk of aspiration then NPO.
▪ If a k/c/o DM and blood glucose >200mg/dL, then give insulin

Anticoagulation

No need to give Heparin. Start on Warfarin directly because the thrombus has already been
cleared.

Complications
▪ Seizures- due to oedema/cortical involvement/hypoglycaemia
▪ DVT- develops 2 to 5 days after haemorrhagic stroke
▪ Pneumonia
o Aspiration- prevent by suction, semi recumbent position, NGT, NPO
o Ventilator associated pneumonia
o Hospital acquired pneumonia
▪ Pressure sores- prevented by air mattress
▪ Catheter associated UTI
 ***Stroke Mimics

TB and Stroke
• TB meningitis causes endarteritis which itself can cause stroke.
• Mycotic aneurysmal rupture causing a bleed.
• Tuberculomas are stroke mimics.
Structural Stroke mimics
• Primary cerebral tumours
• Metastatic cerebral tumours
• Subdural haematoma
• Cerebral abscess
• Neurocysticercosis
• Tuberculoma
• Toxoplamosis
• Peripheral nerve lesions (vascular or compressive)
• Demyelination
Functional Stroke mimics‐ (These are reversible)
• Todd’s paresis- after epileptic seizure
• Hypoglycaemia
• Migrainous aura- with or without headache
• Focal seizures
• Encephalitis
• Meniere’s disease or any vestibular disorder
Feature
Symptom onset
Symptom progession
Severity of deficit
Pattern of deficit
Loss of consciousness
Stroke Stroke mimic
Sudden (minutes) Often slower onset
Rapidly reaches maximum Often gradual onset
severity
Unequivocal May be variable/uncertain
Well defined pattern May be non specific
Less common More common

***Stroke in the young‐ Causes and Work up- (<40 years)

1. Cerebral infarct

• Cardiac embolism (especially in RHD/MS/AF) tell this first- Echocardiography (TEE)

• Premature atherosclerosis- serum lipids
• Arterial dissection- MRI, angiography
• Thrombophilia- Protein C, Protein S, Antithrombin III, Factor V Leiden, Prothrombin 20210
• Homocystinuria- Urinary amino acids
• Neurovascular syphilis- VDRL
• Sickle cell anaemia- HMG with PS, HbS
• APLAb syndrome- Anticardiolipin antibodies
• SLE- ANA
• Vasculitis- ESR, CRP, ANCA
• CADASIL- (Cerebral Autosomal Dominant Arteriopathy with Subcortical Infarcts and
Leukoencephalopathy)

2. Primary intracerebral haemorrhage

• Warfarin toxicity- esp in RHD patients: PT/INR, aPTT
• Arteriovenous malformation- MRI/Angio
• Drug use- Amphetamines, Cocaine
• Sites of haemorrhage
o Putamen
o Thalamus
o Cerebellum
o Pons
 ***Internal capsule anatomy- Anterior limb, genu, posterior limb, retro, sub lentiform parts

up of projection fibres in

terior limb
ei. The fibres arising
tex of the opposite
pathway.

cranial nerves and thus

the opposite half of the

mb. Upper limb fibres

r of the extrapyramidal

striate, corticonigral etc.

fferent directions to

ensations to the cortex.

he capsule and connects

ract
d connects MGB with the
 Arterial supply-

1. Medial and lateral striate branches of MCA‐

• One of the striate branches is larger and is more frequently ruptured. It is called
Charcot’s artery of cerebral haemorrhage.
• It enters through the anterior perforated substance and supplies the posterior
limb of the capsule.
2. Striate branches of ACA
• One of these branches is larger and takes a recurrent course. It is called
Recurrent artery of Heubner. It supplies the anterior limb and genu.
3. Central branches of Anterior choroidal artery- sublentiform
4. Direct branches from internal carotid artery- genu
5. Central branches of posterior communicating artery

Recurrent artery of Heubner infarct‐ Faciobrachial monoplegia

• Tracts involved- corticonuclear in the genu, so paralysis of the face
• Paralysis of the upper limb on the opposite sitde because of involvement of adjacent
pyramidal fibres supplying the upper limb (they are the anterior most)

Ascending and descending tracts and their pathways

Sensory pathways

Dorsal column pathway

• Fine touch
• Vibration
• Proprioception
• Two point discrimination
• Stereognosis
• Tactile localisation
First order neurons- ascend ipsilaterally to the nucleus gracilis (LL) and
nucleus cuneatus (UL) of the medulla.
Second order neurons- Cross in the medulla and ascend to the thalamus.
Third order neurons- Thalamus to somatosensory cortex
Fourth order neurons- Integrate complex information

Anterolateral pathway/Spinothalamic
• Pain
• Temperature
• Crude touch
First order neurons- synapse onto second order neurons in the spinal cord.
Second order neurons- Cross the midline and reach the contralateral
thalamus
Third order neurons- Thalamus to cortex
Fourth order neurons- Integrate complex information
 Fast pain- (ex pin prick) is carried by Aδ, Group II and Group III fibres. It has a
rapid onset and offset and is precisely localised.

Slow pain‐ (ex burn) is carried by C fibres. Characterised by poorly localised

aching/burning/throbbing pain.

Sensory areas
• Primary somatosensory area (S1)- present in the postcentral gyrus. Includes Brodmann’s
areas 3,1,2.
• Primary somatosensory area (S2)- located in the wall of the sylvian fissure
• Somatosensory association cortex- area 5
• Precentral gyrus
Descending (Motor) Tracts

Lateral system pathways‐ descend in the lateral column of the spinal cord. Involved in the
regulation of skilled voluntary movements because they innervate the distal limb muscles.
• Corticospinal tract
• Rubrospinal tract
Medial system pathways- descend down in the medial and anterior columns of the spinal cord.
Involved in the regulation of posture
• Reticulospinal
• Vestibulospinal
• Tectospinal
• Anterior corticospinal

Corticospinal Tract

Origin:
• Primary motor cortex (precentral gyrus, Brodmann area 4)
• Premotor cortex (area 6)
• Supplementary motor cortex (area 6)
• Primary somatosensory cortex (3,1,2)
• Parietal lobe
• Cingulate gyrus
Course
• Fibres converge in the subcortical areas- corona radiata
• Converge through the posterior limb of the internal capsule
• Descend down in the ventral brainstem as the cerebral peduncles
• In the lower medulla, they pass through the pyramid where 80% of the fibres decussate and
descend in the lateral funiculus of the spinal cord forming the lateral CST.
• The remaining 20% descend down ipsilaterally (do not decussate) in the anterior funiculus of
the spinal cord constituting the anterior CST. They cross over only at the spinal cord
segments.
• The lateral CST fibres terminate on the lateral group of motor neurons in the ventral horn of
the spinal cord.
• 30% terminate directly on the motor neurons and 70% terminate through interneurons.
Cortical strokes

• Middle cerebral artery

 o Supplies all of the lateral hemisphere except
▪ The frontal pole and strip along the superomedial frontal and parietal lobes (
ACA)
▪ Lower temporal and occipital pole convolutions (PCA)
o MCA branches
▪ Lenticulostriate branches- penetrating branches of proximal MCA (M1
segment)- supply putamen, globus pallidus externus, posterior limb of
internal capsule, adjacent corona radiata, most of the caudate nucleus
▪ M2 branches- in the sylvian fissure, it divides into superior and inferior
branches
o Manifestations of MCA strokes
▪ Complete MCA stroke
• Contralateral hemiplegia, hemianaesthesia, homonymous
hemianopia
• Dominant hemisphere- global aphasia
• Non-dominant hemisphere**
o Anosognosia- patient is unaware of their disability
o Constructional apraxia- inability or difficulty to
build/assemble/draw objects
o Hemineglect
• Occur when an embolus occludes the stem of the artery
▪ Partial MCA strokes
• Weakness of hand/arm alone
• Facial weakness with Broca aphasia
• Frontal opercular syndrome- Facial weakness+ Aphasia+ arm
weakness
• ACA strokes
o Anatomy
▪ A1 segment- connects the ICA to Anterior communicating artery
▪ A2 segment- distal to A.Comm
▪ A1 segment gives rise to deep penetrating branches that supply the anterior
limb of internal capsule, anterior perforated substance, amygdala, anterior
hypothalamus
o A1 strokes are rare due to collaterals through A.comm
o A2 strokes
 ▪ Unpaired A1 with both A2 branches from a single A1
• Profound abulia- delay in verbal and motor response
• Spastic quadriparesis
• Urinary incontinence- paracentral lobule involvement
▪ Single ACA
• Contralateral leg and foot
• Lesser degree of contralateral arm
• Urinary incontinence
• Frontal lobe symptoms
o Contralateral grasp reflex, sucking reflex- release signs
o Gegenhalten
• PCA strokes
o Anatomy
▪ 75% of PCAs arise from the basilar artery
▪ In 20%, one has its origin from the ipsilateral carotid artery via the P.comm
o Proximal PCA strokes- midbrain stroke syndromes mentioned below-
Weber/Claude/Benedikt
o Distal PCA strokes
▪ Causes infarction of the medial temporal and occipital lobes
▪ Contralateral homonymous hemianopia with macular sparing
▪ Peduncular hallucinosis- hallucinations of brightly coloured scenes and
objects
▪ Bilateral PCA strokes
• Cortical blindness (blindness with preserved pupillary reaction) with
anosognosia- Anton syndrome
• Complicated stuff like
o Balint syndrome
o Palinopsia
o Asimultanagnosia

Lacunar strokes
• Infarction following atherothrombotic or lipohyalinotic occlusion of a small artery in the
brain
• Called so because the thrombosis of these small vessels forms small lakes of fluid or lacunes
in autopsy
• Four characteristic lacunar stroke syndromes
o Pure motor hemiparesis- infarct in the posterior limb of internal capsule
o Pure sensory stroke- thalamic infarct
o Ataxic hemiparesis- ventral pons or internal capsule
o Dysarthria and clumsy hand/arm syndrome- ventral pons or genu of internal capsule
Hypertensive IC haemorrhage
• Most common sites in decreasing order of frequency
o Putamen
o Thalamus
o Cerebellum
o Pons
• Putamen bleed
o Presents with hemiparesis because the bleed in the putamen compresses on the
internal capsule
• Thalamic bleed- also hemiparesis for the same reason. Prominent sensory deficit
 • Pontine haemorrhage- deep coma with quadriplegia over minutes
• Cerebellar haemorrhage- occipital headache, repeated vomiting, gait ataxia

Brainstem strokes

Localisation‐ the rule of 4’s

• 4 cranial nerves in Medulla, Pons, Above Pons (2 in midbrain and 2 above brainstem)
• 4 cranial nerves divide into 12 (3, 4,6, 12)- their motor nuclei are located medially
• 4 cranial nerves do not divide into 12 (5,7,9,11)- their motor nuclei are located laterally
• 4 midline columns- Motor nucleus (of 3,4,6,12), Motor pathway (Corticospinal tract), MLF,
Medial lemniscus (dorsal column pathway)
• 4 lateral (side) columns- Sympathetic, Spinothalamic, Sensory nucleus of V nerve,
Spinocerebellar
• Lesions in all the cranial nerve nuclei cause ipsilateral deficits
• Midline column lesions
o Motor pathway- contralateral weakness
o MLF- ipsilateral INO- Ex: In left INO, when an attempt is made to look right, the left
eye will adduct minimally whereas the right eye will abduct with nystagmus
o Medial lemniscus- contralateral proprioception/vibration loss
• Side structure lesions
o Spinocerebellar tract- ipsilateral ataxia
o Spinothalamic- contralateral pain/temperature loss
o Sensory nucleus of V nerve- ipsilateral loss of pain/temperature in face
o Sympathetic pathway- ipsilateral Horner’s syndrome
• Caveats
o V nerve involvement should not be used to localise to pons, rather to lateral side
o VIII nerve involvement should only be considered as deafness because vestibular
signs can be from the pons or medulla.
Site Eponym Artery Structures affected Differentiating Other
clinical features
features
Lateral Wallenberg PICA 1. Spinothalamic tract IX and X nerve Vertigo and
Medullary 2.Spinocerebellar tract involvement- nystagmus
Syndrome loss of gag due to
 3.Sensory nucleus of V reflex, vestibular
nerve hoarseness, nucleus
4.Horner’s dysphagia, involvement
5.IX and X nerve Ryle’s tube in
situ, Hiccups

Medial Dejerine Vertebral 1.Corticospinal tract XII nerve

medullary artery 2.Medial lemniscus involvement-
syndrome 3.MLF tongue
4.XII nerve deviated to
ipsilateral side
Lateral AICA 1.Spinothalamic tract VII nerve palsy
pontine 2.Spinocerebellar tract
syndrome 3.Sympathetic pathway
4.Spinal nucleus of VN
5.VII N
Medial Paramedian 1.Corticospinal tract VI nerve palsy-
pontine branches of 2.Medial lemniscus Strabismus, LR
syndrome basilar A 3.MLF palsy
4.VI nerve
Ventral Locked in Basilar Quadriplegia,
Bilateral long tract signs
pontine syndrome artery Sometimes aphasia
syndrome supplemented by V-VIII Usually no eye
nerve dysfunction paralysis
Communicate
by eye
movements or
blinking
Medial Weber Penetrating 1.Corticobulbar tract (Does not
midbrain branches of 2.Corticospinal tract exactly follow
syndrome PCA 3.III nerve the rule of 4)
Contralateral
face weakness
due to
corticobulbar
involvement,
III nerve-
ipsilateral eye
down and out
with pupillary
dilation
Lateral Benedikt Penetrating 1.III nerve Red nucleus-
midbrain Claude branch of 2.Red nucleus contralateral
syndrome syndrome PCA 3.Dentatorubrothalamic body
tract Tremor/ataxia-
DRT tract

Dorsal Parinaud Not usually 1.Rostral interstitial Most

midbrain vascular. nucleus of MLF- upward common
syndrome Pinealoma, gaze palsy cause is
MS etc 2. Collier’s sign- eyelid Pinealoma
Viva points
• Causes of recurrent hemiplegia
o Embolic stroke
o Vasculitis
o Demyelination- Multiple sclerosis
o Todd’s paralysis
o Infection
o Hypoglycaemia
• Sudden onset non-vascular aetiology weakness
o Todd’s paralysis- post ictal
o Trauma
• Strokes which can cause quadriparesis
o Stroke in unpaired ACA
o Basilar artery stroke
• Decorticate vs. Decerebrate rigidity
• Hypertensive bleed- Thalamus and Putamen
• Uncal herniation order of weakness
• Lacunar infarcts- read
• Watershed infarcts- caused by hypotension
• Pseudobulbar palsy vs bulbar palsy
• Pseudobulbar palsy causes
o Recurrent stroke
o Multiple sclerosis
o Motor neurone disease
• Inobvious stroke- stroke which is not being recognised as one
o Homonymous hemianopia
o Frontal stroke
o Lateral medullary syndrome- hiccups, vertigo, vomiting