CNS QUESTIONS

1) Classify stroke.
A) 1) TIA-Focal neurological defect of sudden onset resolves within a
period of 24 hours. low flow TIA, embolic TIA, Lacunar TIA, Crescendo
TIA.
2) RIND- Reversible ischemic neurological defecit completely
resolves in 1-3 days.
3) Completed stroke- Rapid onset and persistent neurological deficit
which does not progress beyond 96 hrs.
4) Evolving stroke- There is gradual step wise development of
neurological deficit.
5) Lacunar infarction- Infarction of perforating branch (<1.5 cm
infarct) types- pure motor, pure sensory, sensory and motor, ataxia,
dysarthria,clumpsy hand syndrome.

2) Neurological manifestations of HIV.

A) Space-occupying lesion(s)-Toxoplasmosis, primary CNS lymphoma,
progressive multifocal leucoencephalopathy (PML), TB
Cognitive impairment -AIDS dementia, PML, CMV, syphilis

Encephalitis-HIV, varicella zoster virus, herpes simplex, syphilis

Meningitis- HIV seroconversion, Cryptococcus, TB, syphilis Spastic
paraparesis- HIV-vacuolar myelopathy, transverse myelitis from varicella
zoster, herpes simplex, human T-cell lymphotropic virus 1, syphilis
Polyradiculitis- CMV, non-Hodgkin lymphoma
Peripheral neuropathy - HIV, drugs.
Retinitis - CMV, toxoplasmosis, retinal necrosis, HIV, syphilis

3) Neurosyphilis.
A) Meningovascular (5 years interval from primary infection)
General paralysis of the insane (5-15 years interval from primary
infection)
Tabes dorsalis (5-20 years interval from primary infection)

4) Difference between embolic, haemorrhagic and thrombotic stroke.

A)
Thrombosis Embolic Haemorrhagic
Middle age or elderly Common in young Usually above 40
females years of age
Often hypertensive Source of embolus will Almost all are
with features of be present hypertensive
atherosclerosis
Onset less rapid Develops in seconds. Develops acutely at
usually with stepwise History of TIA may be the height of emotion
progression present. or excitement
Occurs during sleep or Irregular pulse may be Heart may show LVH
soon after getting up present in case of AF due to hypertention
from bed
Mild headache and Headache and Headache, vomiting,
convulsions may occurconvulsions are convulsions present in
usually absent most cases
Carotid bruit may be Evidence of systemic Irregular or cheyne
present embolization may be stokes breathing are
present common.

5) Apraxia.
A) Inability to perform certain purposive movement in the absence of
motor weakness, sensory loss or ataxia. It develops in frontal and
parietal lobe lesions.

6) Features of dominant parietal lesion.

A) Disorder of language, Gerstmann syndrome (defect in calculation,
writing, finger naming, and right to left orientation), tactile agnosia,
bilateral ideomotor and ideational apraxia.

7) Gerstmann's Syndrome.
A) Inability to name body parts, confusion of the left and right sides of
the body, acalculia and agraphia (inability to write).

8) Crossed hemiplegia.
A) Paralysis of ipsilateral cranial nerves(lmn type) with contralateral
hemiplegia. It is a feature of brain stem disease.
Mid brain- upper level- Weber's syndrome.
lower level- Benedikt's syndrome.
Pons- Millard gubler syndrome, Foville's syndrome.
Medulla- Medial and lateral medullary syndromes.

9) Premitive reflex and its importance.

A) These include pout reflex, facial reflex jerks, palmomental reflex,
grasp reflex, utilization behaviour. seen in frontal lobe disease or diffuse
degenerative brain disease.
10) Causes of bilateral bells palsy.
A) GB syndrome, sarcoidosis, Leprosy, Bilateral CSOM, Basal
meningitis, Neuroporphyria, Diphtheria, Lyme disease.

11) Glascow coma scale.

A) Eye-opening (E) • Spontaneous 4 • To speech 3 •
To pain 2 • Nil 1
Best motor response (M) • Obeys 6 • Localises 5 •
Withdraws 4 • Abnormal flexion 3
• Extensor response 2 • Nil 1 Verbal
response (V) • Orientated 5 • Confused conversation 4 • .
Inappropriate words 3 • Incomprehensible sounds 2 •
Nil 1
Coma score = E + M + V
• Minimum 3 • Maximum 15

12) Cruciate hemiplegia.

A) Paresis or paralysis of ipsilateral lower limb and contralateral upper
limb. This is because arm fibres cross before the leg fibres at lower part
of medulla.

13) Uncomplicated hemiplegia.

A) Hemiplegia with no cranial nerve involvement.

14) Mini mental state examination.

A) 5 ( ) What is the (year) (season) (date) (day) (month)?
5 ( ) Where are we (country) (county) (town/city) (building) (floor)?
Registration 3 ( ) Name three common objects (e.g. 'apple', 'table',
'penny'). Take 1 second to say each. Then ask the patient to repeat all
three after you have said them. Give 1 point for each correct answer.
Then repeat them until he/she learns all three. Count trials and record.
Trials ( )
Attention 5 ( ) Spell 'world' backwards. The score is the number of letters
in the correct order. (D_L_R_O_W_)
Recall 3 ( ) Ask for the three objects repeated above. Give 1 point for
each correct answer. (Note: recall cannot be tested if all three objects
were not remembered during registration) Language 2 ( ) Name a
'pencil' and a 'watch'. (2 points)
1 ( ) Repeat the following: 'No ifs, ands or buts.' (1 point)
3 ( ) Follow a three-stage command: 'Take this paper in your right hand,
fold it in half, and put it on the floor.' (3 points)
1 ( ) Read and obey the following: (1 point) CLOSE YOUR EYES
1 ( ) Write a sentence. (1 point)
1 ( ) Copy the following design. Give 1 point if no construction problem
(intersecting pentagon).

30 ( ) Total Examiner __________________

The Mini-Mental State Examination (MMSE) is a useful screening
questionnaire to detect cognitive impairment. A score of less than 24 out
of 30 indicates cognitive impairment.

15) Horner's syndrome.

A) Involvement of the sympathetic fibres which originate from the
hypothalamus pass down the brain stem and cervical spinal cord to
emerge at T2, return back up in association with internal carotid artery
and supply the dilator pupillae.
components: Miosis, Ptosis, Enophthalmos, Anhidrosis.
Causes: Massive CVA, Syringobulbia, lateral medullary syndrome,
syringomyelia, tumour of internal carotid artery, carcinoma of apex of
lung, pancoast tumour, cervical rib.

16) Grading of tendon reflexes.

A). 0- Absent
1- Present
2- Brisk
3- Very brisk
4- Clonus.

17) Re enforcement manouver.

A) Ask the patient to interlock the flexed fingers of his hands and pull one
against the other while simultaneously eliciting the reflex.
this increases the excitability of anterior horn cells.

18) past history relavent in cns

A) h/o TIA, Head injury, exposure to STD, Hypertention, Diabetes,
Epilepsy, Tuberculosis, intake of OCP's, Dyspnoea, Intermittent
claudication, weight loss.

19) Causes for predominant proximal muscle weakness?

A) Predominantly proximal weakness suggests a primary muscle disease,
such as immune-mediated inflammatory muscle disease, e.g.
dermatomyositis or polymyositis, or a non-inflammatory myopathy, e.g.
secondary to chronic alcohol use, steroid therapy or thyrotoxicosis.
painless: myopathy, GB syndrome, Muscular dystrophies.
Painfull: polymyositis, Diabetic amyotrophy.

20) Different types of sensory disturbances?

 a) Dissociated anaesthesia.
A) Seen in central cord lesion such as syringomyelia, there is
affection of spinothalamic tract due to involvement of fibres crossing the
cord from both sides in the anterior commissure though it spares the
posterior column. Thus touch sensation persists but pain and temperature
is lost below the level.

b) Glove and stocking type of sensory disturbance.

A) Seen in peripheral neuropathy. affects distal parts more, involves
all modalities of sensation.

c) root pain
A) Dermatological pattern of pain, pain is more felt than loss of
sensation.Due to nerve root involvement.

d) rombergism
A) Sensory ataxia due to loss of joint position and vibration sense due
to involvement of posterior tract.

e)tight band like sensation

A) Seen when there is spinal canal involvement.

f) lhermitt sign
A) Sharp shooting pain felt down the neck on full flexion of neck seen
in cervical spondylosis, Multiple sclerosis.

g) funicular pain.
A)Burning or lancinating pain felt in an area of decreased or absent
sensation. Commonly see in patients with spinal cord involvement.

21) TIA
A) Focal neurological defecit of sudden onset lasting for less than 24
hours occuring due to abnormality in the vasculature or its contents.

22) Argyrl robertson pupil.

A) Accommodation reflex is present but light reflex lost.
usually bilateral involvement but more markedon one side, dilates
slowly to mydriatics.
seen in association with: neurosyphilis, Amyloidosis, Diabetes mellitus,
Multiple sclerosis, Pinealomas, Wernicke's encephalopathy.

23) Bells phenomenon.

A) The eyeball rolls upward and inwards during attempted forced eye
closure. seen in normal and also in LMN type of 7th nerve palsy.
24) Cosequenses of long standing facial palsy.
A) Exposure keratitis, facial hemispasm, facial contracture, crocodile
tears, jaw winking.

25) Direction of nystagmus.

A) Horizontal nystagmus- It is to and fro movement of eyeball in a
horizontal plane.It is seen in following conditions: vestibular nerve
lesion, vestibular nuclei lesion, lesion of the median longitudinal bundle,
lesion of the cerebellum.
Vertical nystgmus: It is up and down movement of the eyeball in vertical
plane. It is seen in following conditions involving the brain stem:
Vascular accident, encephalitis, multiple sclerosis, syringobulbia,
wernicke'sencephalopathy.
Rotatory nystagmus: It is an oscillatory movement of the eyeball which
is rotatory in character. It is seen in labyrinthine disorders.

26) Gag reflex.

A) contraction of pharyngeal muscles on touching the posterior
pharyngeal wall.
Afferent is 9th nerve,efferent is 10th cranial nerve.

27) Defenition and difference between UMN and LMN.

A)
UMN LMN
Site of lesion From cortex till At or below anterior
anterior horn cell horn cell
Affects Muscle group Individual muscles
Tone Clasp knife spasticity Flaccidity
DTR Brisk Absent
Muscle bulk Disuse atrophy Wasting
Plantar reflex Extension flexion

28) Causes for muscle enlargement.

A) true hypertrophy seen in workers in heavy occupation, athletes.
Pseudo hypertrophy seen in duchenne muscular dystrophy.
Enlargement of muscle is also seen in certain myotonic disorders.

29) Gower's sign.

A) Person uses the arms to climb up the legs while getting up from sitting
or lying down possition due to proximal muscle weakness. ex: DMD.
30) Baevor's sign.
A) When lower part of rectus abdominis muscle is paralysed, the
umbilicus moves upwards on raising the shoulders from bed. This sign is
seen in the nerve lesions between 8th and 11th thoracic segment.

31) Abnormal movements.

A) Fasciculation
Fasciculation looks like irregular ripples or twitches under the skin
overlying muscles at rest. This occurs in lower motor neurone disease,
usually in wasted muscles. Flick the skin over wasted muscle to try to
elicit fasciculation. Non-pathological fasciculation is common in healthy
people and not associated with weakness or wasting.
Myoclonic jerks
These are sudden shock-like contractions of one or more muscles which
may be focal or diffuse and occur singly or repetitively. Healthy
individuals commonly experience these when falling asleep. They may
also occur in association with epilepsy, diffuse brain damage and
dementias.
Tremor
Tremor is an oscillatory movement about a joint or a group of joints
resulting from alternating contraction and relaxation of muscles. Tremors
are described according to their speed (fast or slow), amplitude (fine or
coarse) and whether they are maximal at rest, on maintaining a posture
or on carrying out an active movement.

Physiological tremor is a fine, fast postural tremor seen with anxiety. A

similar tremor occurs in hyperthyroidism and with excess alcohol or
caffeine intake, and is a side-effect of β-agonist bronchodilators used in
asthma and chronic obstructive pulmonary disease (COPD)

Essential tremor is the most common cause of an action tremor, typically

affecting the upper limbs and sometimes the head, with a postural and
action component. It may be reduced by alcohol, and often demonstrates
an autosomal dominant pattern of inheritance

Action tremors, which are coarse and even violent, are associated with
lesions of the red nucleus (rubral tremor) and subthalamic nucleus. They
are most often caused by cerebrovascular disease or multiple sclerosis
Parkinson's disease demonstrates a slow, coarse tremor, which is worst at
rest but reduced by voluntary movement. It is more common in the upper
limbs and usually asymmetrical

Intention tremor is absent at rest but maximal on movement, and is

usually due to cerebellar damage. It can be assessed with the finger-nose
test
Other involuntary movements (dyskinesias)

These are classified according to their appearance:

 Dystonia is caused by sustained muscle contractions, leading to
twisting, repetitive movements and sometimes tremor
 Chorea and athetosis are both writhing movements. The former
tends to be irregular, jerky and brief; the latter is slower and more
sustained. They are often combined, when they are called
choreoathetosis.
 Ballism refers to violent flinging movements caused by
contractions of proximal limb muscles, sometimes affecting only
one side of the body (hemiballismus)
 Tics are repetitive, stereotyped movements which can be briefly
suppressed by the patient.

32) Sensory pathways.

A)
Dorsal Column-Medial Lemniscal System
1. Touch sensations requiring a high degree of localization of the
stimulus
2. Touch sensations requiring transmission of fine gradations of
intensity
3. Phasic sensations, such as vibratory sensations
4. Sensations that signal movement against the skin
5. Position sensations from the joints

6. Pressure sensations related to fine degrees of judgment of pressure

intensity
Anterolateral System
1. Pain
2. Thermal sensations, including both warmth and cold sensations
3. Crude touch and pressure sensations capable only of crude
localizing ability on the surface of the body
4. Tickle and itch sensations

5. Sexual sensations

33) Saddle anaesthesia.

A) Occurs in cauda equina or conus medularis lesion. Sensation over the
lower sacral segments are impaired. All forms of sensation are impaired,
lower limbs reflexes and bladder control are usually lost in patients with
saddle anaesthesia.
34) Sacral sparing.
A) Sensation is preserved in the distribution of sacral dermatome. Seen in
intra medullary lesion in the upper thoracic or cervical cord. There will
be sparing of laterally located fibres in the spino thalamic tract carrying
sensation from the sacral segment.

35) Superficial reflexes.

A) These are polysynaptic reflexes and the brain has an excitatory effect
on them and hence they are absent in UMN Type of lesion.

An abnormal plantar response (S1-2) is extension of the large toe

(extensor plantar response), often accompanied by flexion and abduction
of the other toes (Babinski response). This is an unequivocal sign of
upper motor neurone damage and is usually associated with spasticity,
clonus and hyper-reflexia.

Superficial abdominal reflexes (T8-12) are lost in upper motor lesions

but will also be affected by lower motor neurone damage affecting T8-12.
They may be difficult to elicit in the obese, the elderly or those who have
had abdominal surgery.

The cremasteric reflex (L1 and L2) is used to assist in identifying the
level of spinal cord lesions, particularly after injury.

36) Extensor plantar response causes other than UMN.

A) Infants below one year,
Comatose Pt,
After epileptic fit, Deep sleep.

37) Deep tendon reflexes.

 A) Biceps: (C5, C6). With the patient seated, lie their arms across
their abdomen. Place your thumb across the biceps tendon and
strike it with the tendon hammer as above. Watch the biceps for
contraction.
 Supinator: (C5, C6). The muscle tested is actually the
brachioradialis. With the patient's arms lying loosely across their
abdomen, put your fingers on the radial tuberosity and tap with the
hammer. The arm will flex at the elbow. If brisk, the fingers may
also flex.
 Triceps: (C7). Taking hold of the patient's wrist, flex their arm to
~90°. Tap the triceps tendon about 5cm superior to the olecranon
process of the ulna. Watch the triceps.
  Fingers: (C8). This is only present if tone is pathologically t. With
your palm up and the patient's arm pronated, lie their fingers on
yours. Strike the back of your fingers. The patient's fingers will
flex.
 Knee: (L2,L3, L4). With the patient's leg extended, use one hand
behind their knee to lift their leg to ~60°. Tap the patella tendon
and watch the quadriceps. If brisk, proceed to testing for clonus
here:
o Knee clonus: with the patient's leg extended, place your
thumb and index finger over the superior edge of the patella.
Create a sudden downward (toward the feet) movement, and
hold. Watch the quadriceps. Any beat of clonus here is
abnormal.
 Ankle: (S1, S2). With the hip flexed and externally rotated and the
knee flexed to ~90°, hold the foot and tap the Achilles tendon.
Watch the calf muscles for contraction/ankle flexion.

38) Neuronal/spinal shock.

A) Usually spinal cord lesions produce features of UMN lesions below
the level of lesion.
But in severe spinal cord injury, there is complete suppression of all
spinal segmental reflex activity, below the level of lesion resulting in
LMN type of features below the level of lesion.This is a state of spinal
shock.
This state may last for days to weeks.

39) Mass reflex.

A) An abnormal condition, seen in patients with transection of the spinal
cord, characterized by a widespread nerve discharge. Stimulation below
the level of the lesion results in flexor muscle spasms, incontinence of
urine and feces, priapism, hypertension, and profuse sweating.

40) cerebellar lobe and its functions.

A) Anatomically, the cerebellum is divided into three lobes by two deep
fissures (1) the anterior lobe,
(2) the posterior lobe, and
(3) the flocculonodular lobe. The flocculonodular lobe is the oldest
of all portions of the cerebellum; it developed along with (and
functions with) the vestibular system in controlling body equilibrium.
Note down the center of the cerebellum a narrow band called the vermis,
separated from the remainder of the cerebellum by shallow grooves. In
this area, most cerebellar control functions for muscle movements of the
axial body, neck, shoulders, and hips are located.
To each side of the vermis is a large, laterally protruding cerebellar
hemisphere, and each of these hemispheres is divided into an
intermediate zone and a lateral zone.
The intermediate zone of the hemisphere is concerned with controlling
muscle contractions in the distal portions of the upper and lower limbs,
especially the hands and fingers and feet and toes.
The lateral zone of the hemisphere operates at a much more remote level
because this area joins with the cerebral cortex in the overall planning of
sequential motor movements. Without this lateral zone, most discrete
motor activities of the body lose their appropriate timing and sequencing
and therefore become incoordinate

41) Difference between intra and extramedullary lesions of

spinal cord.
A)
Feature Extramedullary Intramedullary
Root pains Common Rare
Dissociate anaesthesia Uncommon Common
Pyramidal signs Marked Not so marked
Wasting Minimal Marked
Brown sequard May occur Does not occur
syndrome
Sphincter disturbance Late Early
Trophic changes Minimal Marked
Spinal tenderness May be present Usually absent
CSF proteins Raised Normal
Lhermitte’s sign Present Absent

42) Difference between cauda equina and conus medularis and its
lesion.
A)
FEATURE CONUS MEDULARIS CAUDA EQUINA
Anatomy It is the distal most It is a collection of
part of the spinal cord nerve root below the
conus.It contains nerve
roots from L1-L5 and
S1-S5
Presentation Sudden and bilateral Gradual and
unilateral
Reflexes Knee jerks preserved Both ankle and knee
but ankle jerks jerk affected.
affected
Radicular pain Less severe More severe
Low back pain More Less
Sensory symptoms and Numbness is Numbness is
signs symmetric, and asymmetric, may be
bilateral, sensory unilateral,No sensory
dissociation occur. dissociation
Motor strength Typically symmetric, Asymmetric, areflexic,
hyperreflexic distal paraplegia.
paresis of lower limbs
Impotence Frequent Less frequent
Sphincter dysfunction Overflow urinary Urinary retention
incontinence and fecal tends to present late in
incontinence, tend to course of disease.
present early in course
of disease

43) classification of spinal cord diseases.

A) 1) compressive myelopathy: a) Extra medullary: 1) Extra dural
2) Intra dural
b) Intra medullary.
Causes: Epidural, intradural, or intramedullary neoplasm
Epidural abscess
Epidural hemorrhage
Cervical spondylosis
Herniated disk
Posttraumatic compression by fractured or displaced vertebra or
haemorrhage
2) Non compressive myelopathy

Vascular

Arteriovenous malformation
Antiphospholipid syndrome and other hypercoagulable states

Inflammatory

Multiple sclerosis
Neuromyelitis optica
Transverse myelitis
Sarcoidosis
Sjögren-related myelopathy
Systemic lupus erythematosus
Vasculitis

Infectious
 Viral: VZV, HSV-1 and -2, CMV, HIV, HTLV-I, others
Bacterial and mycobacterial: Borrelia, Listeria, syphilis, others
Mycoplasma pneumoniae
Parasitic: schistosomiasis, toxoplasmosis

Developmental

Syringomyelia
Meningomyelocele
Tethered cord syndrome

Metabolic

Vitamin B12 deficiency (subacute combined degeneration)

Copper deficiency
Toxic
Arsenic, lathyrism

44) Invertor of radial (supinator).

A) The inverted supinator (brachioradialis) reflex is a sign that was
introduced into clinical medicine by Babinski (1910). Since that time, it
has been widely accepted as signifying a lesion at the C5-C6 spinal cord
segments. There are two components of this abnormal reflex: (1) an
absence of contraction of the brachioradialis muscle when the styloid
process of the radius is tapped, and (2) a hyperactive response of the
finger flexor muscles; a response that is subserved by a lower spinal cord
segment (C8).

45) Invertor of biceps.

A) On eliciting the biceps jerk, there is no flexion at the elbow, but
instead there is extension at the elbow due to contraction of the triceps
muscle and there is brisk finger flexion along with thumb adduction.
Presence of this reflex indicates that the lesion is at the level of C5.6
segment.

46) Invertor of knee.

A) On eliciting the knee jerk, there is no extention of the knee, but instead
there is flexion of the knee due to contraction of the hamstring muscles.
Presence of this reflex indicates that the lesion is at the level of L2,3,4
segment.

47) palpation of peripheral nerves.

A) Enlarged peripheral nerves are very rarely found except in
leprosy. Other conditions which could present enlarged peripheral
nerves are: primary amyloidosis and some hereditary peripheral
neuropathies (like the neuropathy of Charcot-Marie-Tooth). These are
all very uncommon.
Nerves that can be palpated in such conditions are: Supra orbital,
greater auricular, Ulnar nerve, radial cutaneous nerve, Median nerve,
common peroneal nerve, Superficial peroneal nerve, Sural nerve and
Posterior tibial nerve.

48) Signs of extra pyramidal disorders.

A) Gait abnormalities, Ataxia, Rigidity, Abnormal movements/
Hypokinesia.

49) Other methods of demonstration of babinski.

A) 1)Oppenheim reflex: A firm stroke with the finger and thumb is
applied down either side of the anterior border of the tibia, greater
pressure being applied to the medial side.
2)Gordon reflex: Calf muscles are squeezed.
3)Chaddock reflex: A light stroke is applied below the lateral malleolus.
4) Gonda's sign is a clinical sign in which flexing and then suddenly
releasing the 4th toe elicits an extensor plantar reflex
5)Schaeffer’s sign: squeeze the achille’s tendon.
6) Bing's sign or Bing's reflex is a clinical sign in which pricking the
dorsum of the foot or toe with a pin causes extension of the great toe

50) Aphasia and its types.

A) Disturbance in the comprehension or production of language in
written or spoken forms.
Types:Sensory/receptive/wernicke’s aphasia
Motor/Broca’s/expressive aphasia
Conduction aphasia
Global aphasia
Transcortical aphasia

51) Common lacunar syndrome.

A) Lacunar stroke or lacunar infarct (LACI) is a type of stroke that
results from occlusion of one of the penetrating arteries that provides
blood to the brain's deep structures. Patients who present with symptoms
of a lacunar stroke, but who have not yet had diagnostic imaging
performed may be described as suffering from Lacunar Stroke
Syndrome (LACS).
Ex: Pure motor stroke/hemiparesis (most common lacunar syndrome:
33-50%)
Ataxic hemiparesis (second most frequent lacunar syndrome)
Dysarthria/clumsy hand(sometimes considered a variant of ataxic
hemiparesis, but usually still is classified as a separate lacunar syndrome)
Pure sensory stroke
Mixed sensorimotor stroke

52) Neurocutaneous markers.

A) a) Adenoma sebaceum: Are actually angiofibromas- reddish pink
greasy nodules. Found in patients with tuberous sclerosis on cheek and
nasolabial folds.
b) Café-au-lait spots: dark brown or light coloured patches
associated with generalized neurofibromatosis. Presence of either more
than 6 spots (5mm) or a single spot exceeding 1.5 cm in diameter is
clinically significant.
c) Shagreen patch: Plaque like lesions usually present in the
lumbosacral area varying from 1- 10 cms. Found in patients with
tuberous sclerosis.
d) Neurofibroma: firm discrete nodules attached to a nerve.
e) Telengiectasia: present in skin, mucosa, gastrointestinal tract,
spinal cord, and brain can be associated with familial
telangiectasia(osler rendu weber disease). Telengiectasia in the bulbar
conjunctiva is associated with cerebellar degeneration( Ataxia
telangiectasia)
f) Vascular nevus: Nevus covers the large part of face and cranium
associated with angiomas of brain (sturge weber syndrome)
g) Low hairline: Posterior hairline is below the C4 vertebra,
associated with cranio vertebral anomalies.
h) Short neck: Ratio of the length of the body to the length of the neck
is more than 13:1. Short neck is associated with cranio vertebral
anomalies.
i) Pes cavus and kyphoscoliosis: Associated with hereditary
neurological disorders.(eg: Freidrich’s ataxia) and also intra spinal
disorder like syringomyelia.
j) Presence of hairs, lipoma or dimple in the skin over the spine is
associated with spina bifida occulta.

53) Site of lesion and type of defficit in motor system.

A) Cortex: Monoplegia or loss of function controlled by that area of
cortex.
Internal capsule: contralateral hemiplegia.
Brain stem: Crossed hemiplegia.
Spinal cord: Ipsilateral weakness or paralysis below the level of lesion
with no cranial nerve involvement.
Peripheral nerve: Weakness and wasting of muscle supplied by the nerve.

54) Blood supply of internal capsule.

A) The superior parts of both the anterior and posterior limbs and
the genu of the internal capsule are supplied by the lenticulostriate
arteries, which are branches off of the M1 segment of the middle cerebral
artery.
The inferior half of the anterior limb is supplied via the recurrent artery
of Heubner, which is a branch of the anterior cerebral artery.
The inferior half of the posterior limb is supplied by the anterior choroidal artery, which is a
branch of the internal carotid artery.

MCA
ACA Posterior communicating artery Anterion choroidal artery

55) Different types of gait.

A) a) Circumduction gait (hemiplegic gait): This type of gait is seen in
hemiparesis. The patient throws his lower limbs outwards, the movement
occurring at the hip joint, producing the movement called circumduction
and leaning forward the opposite healthy side. The affected arm is
adducted at the shoulder and flexed at the elbow, wrist and fingers.
b) Spastic gait(bipyramidal lesion): This type of gait is seen in
lesions of the upper motor neuron involving both the lower limbs. There
is an adductor spasm causing the legs to cross each other and each foot
trips the other. When the adductor spasm is marked, as seen in cerebral
diplegia, the gait is known as scissors gait line. The movements are slow
and stiff. The steps are short with the feet scraping the floor.
c) High stepping gait(foot drop): this type of gait is seen in patients
with foot drop. The patient raises the foot high in order to overcome the
foot drop and on keeping the foot down, the toe hits the ground first.
There is no ataxia.
d) Stamping gait: This type of gait is seen in patients with posterior
column lesion, where there is gross loss of position sense. The patient
does not know where his foot is, and so, on walking raises his foot high
up in the air and brings it down on the ground forcefully(stamping), the
heel of the foot coming in contact with the ground first. This abnormal
gait is more prominent in the dark or when the patient walks with his eyes
closed.
e) Ataxic gait (cerebellar lesion): This type of gait is seen in patients
with cerebellar lesion. The patient is ataxic and reels in any direction,
including backwards and walks on a broad base. The patient finds
difficulty in executing tandem walking.
f) Festenant gait(Extrapyramidal lesion) : This type of gait is seen in
patients with lesions of the extrapyramidal system, associated with
rigidity. The patient makes a series of small, flat footed shuffles. This gait
is typically seen in parkinsonism, where the patient has a stooped posture
and walks rapidly with short, shuffling steps, as if trying to catch up with
gravity. The automatic associated upper limb movement are absent.
g) Waddling gait (Primary muscle disease): This type of gait is seen
in patients with proximal muscle weakness of the lower limbs or with
bilateral hip problem. The patient walks on a broad base with an
exaggerated lumbar lardosis.
h) Apraxic gait: Sequence and composition of movement is lost seen
in bilateral frontal lobe disease.

56) Division of sensory system.

A) Almost all sensory information from the somatic segments of the body
enters the spinal cord through the dorsal roots of the spinal nerves.
However, from the entry point into the cord and then to the brain, the
sensory signals are carried through one of two alternative sensory
pathways: (1) the dorsal column-medial lemniscal system or (2) the
anterolateral system.

57) Ellsberg phenomenon.

A) In cervical compressive myelopathy first there is weakness of
ipsilateral arm then ipsilateral leg then contralateral leg and lastly
contralateral arm occur. this 'u' shaped involvement of limbs is called as
elsberg phenomenon.

58) Cranio vertebral anomalies.

A) 1) Skeletal anomalies:a) Platybasia
b) Basilar invagination- primary or
secondary
c)occipitalisation of atlas.
d) Klippel feil anomaly.
e) Atlanto axial dislocation.
2) Neuraxial anomalies a) Arnold chiari malformation.
b) Dandy walker syndrome.
c) Occipitocervical meningomyelocele
d) Cyst in posterior fossa.
3) Combined skeletal and neural anomalies.

59) Speech problems.

A) Disturbance of articulation is dysarthria.
Impairment of voice or sound production from the larynx is dysphonia.
In both cases language function is intact, but patients' intelligibility may
be a problem. They understand what is being said and the grammatical
construction of their speech is normal.
When language areas in the dominant hemisphere are damaged, there is
disturbance of understanding and/or expression of words. This is
dysphasia.

60) Cortical causes of paraplegia.

A) Cerebral diplegia, superior sagittal sinus thrombosis, parasagittal
meningioma, thrombosis of unpaired anterior cerebral artery.