C ENTRAL N ERVOUS S YSTEM

HISTORY OF PRESENT ILLNESS1. Loss of Consciousness / Drowsiness

2. Convulsions

3. Headache

4. Vomiting

5. Deviation of angle of Mouth, Dribbling of Saliva & Inability to Close

Eyes

6. Inability to speak

7. Difficulty in swallowing, Hoarseness of voice, Nasal Regurgitation,

Nasal Twang, Dysarthria

8. Smell – loss

9. Vision – h / o Double vision, Dimness, Loss

10.Inability to Chew / Numbness over face

11.VIII nerve signs- Tinnitus, Giddiness, Vertigo, Hyperacousis,

Deafness

12.Weakness / inability to use limbs

Both upper limbs (UL),

One half of the body (hemiplegia)

Both LL (Paraplegia)

All 4 limbs (Quadriplegia)

Ask for

Onset – Sudden / within few hours / days / weeks / months

(Gradual)

Progression – progressive / Static / Improving

Triggering factors – Sleep, Exercise, Posture, Reading,

Cough, Eating, Micturition, Stimuli like Light,

Sound, Smell, Heat & Cold

13.Wasting / thinning of limbs

14.Inability to get up / squat

15.Difficulty in Eating, Combing, Buttoning, Walking (daily activities)

16.Difficulty in Writing, Sewing (fine motor skills)

17.Abnormal movements -Inability to wear Chappals/ Chappals falling

off from foot, involuntary movements

18.Gait – dragging the limb / broad –based / high stepping, slowness,

Railing on to one side while walking, Unsteadiness of gait

19.Abnormal Sensations- Numbness & Tingling of Extremities, Feeling

of Walking on Cotton Wool

20.H /o Root Pain with radiation / constricting pain around any area

21.Micturition – inability to pass urine / Fullness of bladder/ Retention

with overflow

22.Defecation – urgency , frequency & h/o Fecal Incontinence

ETIOLOGICAL HISTORY

Ask for history of 1. Trauma / fall (head injury)2. Cough with Expectoration3. Hemoptysis4. Chest pain & Breathlessness5. Ear discharge6. Fever – associated exanthema7. Drug intake- Oral Contraceptives, Phenothiazines, INH,

Ethambutol, Vincristine8. Joint Pain9. Bleeding Diathesis10. HT, DM11. Vaccination, Dog bite (for paraplegia)

PAST HISTORY:1. Head/ Spinal injury2. Infections – TB, Encephalitis, Sepsis3. Rheumatic fever (joint pain)4. h/o STD Exposure, Discharge from Urethra, penile ulcer

5. h/o Recurrent Abortions/ Still births (STD)6. Similar Episodes before7. any Surgery / Drug therapy/ Vaccination8. Ear discharge9. Natal history- full term/ premature, normal/ instrumental10. Postnatal history- Jaundice, Infection, Convulsions, Seizures,11. Infancy- injury

FAMILY HISTORY:DM, HT, TB, Seizures & similar illness

PERSONAL HISTORY:Veg / non-veg, Smoker, Alcohol, Ganja, LSD addiction, Tobacco chewing, Marital status

OCCUPATIONAL HISTORY: Exposure to Toxic chemical – neuropathy, Encephalopathy Prolonged visual work under artificial light – tension headache &

irritation Overuse of certain joints – carpal tunnel syndrome

P HYSICAL E XAMINATION

A. GENERAL EXAMINATION:1. Consciousness2. Comfortable / not 3. Built, nutrition, stature, short neck4. Fever 5. Skull- Shape & size, any Depression/ Bulge/ Scar, Bulging

Fontanelle

6. Hair- low hair line, alopecia, texture (soft/ coarse/ normal)

7. Eyes- color of conjunctiva (blue), Bitot’s spot, Phlycten, sub-

conjunctival

Hemorrhage, KF ring, Icterus, Exopthalmos/ Enopthalmos

8. Eye lids- ptosis (complete/ partial), Absence of closure of eye lid

9. Anemia, Polycythemia, Cyanosis, Clubbing, LN

10. Oral cavity – angular stomatitis (Avitaminosis), Bleeding gums

11. Hematological signs- Petecheae, Purpura, Ecchymosis, Erythema

12. Lower limb – Calf muscle hypertrophy, edema of feet, foot

deformity (Equinovarus/ club foot)

13. Neurocutaneous markers

i. Haemangioma, Facial angiofibroma, Ash leaf shaped

hypopigmented patch (tuberous sclerosis)

ii. Neurofibromas, Lisch Nodules, Café ‘au Lait (light

coffee) Spots (neurofibromatosis)

iii. Oculocutaneous telangectasia (blood shot conjunctiva) –

Ataxia telangectasia

14. Thickened nerves, Trophic ulcers, Joint swelling

15. Spine – Kyphoscoliosis, Gibbus, Meningocele, Pilodinal sinus

16. Examination of breast

B. NEUROLOGICAL EXAMNATION 1. Higher functions

a. Consciousness & perception : find if patient is in Coma / Stupor / Delirium; find out any perception disorder

Consciousness disorders Coma state of unconsciousness in which patient does not respond to

any type of external stimuli / inner needsDeep coma = coma + absence of corneal & conjunctival reflexesSemicoma = arousable with preserved reflexes

Stupor state of disturbed consciousness where patient shows some response to vigourous external stimuli like pain

Disorientation conscious but muddled in time, place & personDelirium state of confusion with excitement & hyperactivityAkinetic mutism

patient is awake but lacks impulse to speak / action

Dementia Acquired global/ multifocal impairment of Cognitive function in presence of normal Consciousness

Locked-in syndrome

Global paralysis of limbs & cranial musculature, patient is receptive but unresponsive

Lesions Clouding of consciousness may be due to

1. Acute cerebral dysfunction (Cerebral hypoperfusion, metabolic disease, Encephalitis)

2. Focal lesions of thalamus esp. if medial & bilat. cause Delirium3. Lesions of Brain stem Reticular activating System

Perception disorders 1. Delusion – false beliefs [eg: he feels that he has cancer]

Common in schizophrenia, GPI, depression2. Hallucinations – false perception of sensations [ringing ears when no sound,

seeing something which doesn’t exist] Hallucinations before the attack of migraine Grandiose delusion in GPI 3. Illusion- misinterpretation of stimuli 4. Obsession – recurrent & persistent thoughts that intrude in pt’s mind despite best efforts to get rid of them

b. Appearance & Behaviour (noticed as the patient walks in)

Appearance- way of dressing, personal hygieneBehaviour – disturbed / apathic/ Agitated / Confused

c. Emotional state

Elated, Euphoric, Excited / DepressedEmotional incontinence – Pseudobulbar palsy, organic dementia, multiple Sclerosis, Cerebral atherosclerosis

d. Cognitive functions

1. Speech & language:

communication problem are obvious while talking to patient.

Find out the type of problem – aphasia / Dysarthria / Dysphonia

Disorder name Defect Causes Dysarthria Speech

pronunciation problem

i. Bulbar palsy – difficulty in consonants (“p”, “t”, “k”)ii. Cerebellar Disease – “scanning” & Robotic speech. Syllables pronounced individuallly (ask pt. to say “Eye- ay”)iii. Pseudo bulbar palsy – “strangled” & spastic speech, Difficulty with tongue twisters (“British constitution” as “brizh conshishushon”)

Dysphonia Loss of voice Laryngeal disease / innervation defectQuiet voice => poor ventilatory capacityFatiguing voice => in Myasthenia gravis, Parkinsonism (slow monotonous speech)

Aphasia Loss/ diffuculty in production & comprehension of spoken/ written language / both

(Refer below for causes)

Aphasia:Type Lesion Characteristics

Motor aphasia / Broca’s aphasia(failure of motor aspects of speech & writing)

Lesions at inferior frontal convolution of left hemisphere [broca’s area]Large lesion involves Cortical & sub Cortical structures of Frontal & Superior Sylvian fissure including Insula [upper division of it mca territory]

Poorly articulated & Non- fluent speech with Reduced no. of words & errors of syntax & grammar (telegraphic speech)

Sensory aphasia / wernicke’s aphasia

posterior parieto-temporal region Impaired comprehension of spoken & written languageFluent speech devoid of meaning (jargon aphasia)Unawareness of speech deficit

Conduction aphasia

Perisylvian area with damage to fibres of arcuate fasciculus

Inability to repeat phrases /words spoken by examiner with normal fluency & comprehension

Transcortical Motor – antrsuprr to Broca’s areaSensory – postrinfrr to Wernicke’s area

Same as brocas & wernicke’s respectively

Global Large lesion of middle cerebral artery’s area / l tint. Carotid artery/ trauma

Marked elements of both broca’s & wernicke’s aphasia

Methods of testing

i. Assess output of speech & fluencyii. Naming of shown objects [eg: pen, comb]

iii. Ask to carry out commands like pick up the penciliv. Repetition of spoken wordsv. Writing – find if error inform, grammer, syntax

2. Memory – past & present Memory How to test Remote memory

marriage date, mother or father’s birth date / job / school’s name, / school mate’s name

Recent memory Ask about the day & what breakfast he had? Tell a short story & ask to recall after 3-5 mins

Short term memory

Ask to repeat the numbers / names & in reverse order. Show pictures & ask to recall after few mins

3. Orientation: Time – ask the patient to tell year, date, month, day, morning /

evening Place – hospital / house, city

Person – able to identify

4. Intelligence This is tested based on the following criteria

i. Abstract thinking – ask pt to explain meaning of common proverb

ii. Reasoning- ask pt to compare objects/ differentiate between a lie & a truth

iii. Judgement – “what pt does on seeing house on fire?”

iv. Attention – ask pt to sequentially subtract 7 from 100 down to 0

v. Calculations – solve simple numerical problems

e. visuospatial fntns Pt is asked to copy a drawing of 5 pointed star / 3

dimensional box

Constructional apraxia / visuospatial agnosia results in difficulty in drawing lines needed in correct spatial correlation

Apraxia Defect in ability to carry out known motor acts in absence of motor weakness/

sensory loss / ataxia Seen in damage of left parietal cortes / parietal white fibres of lt or both

hemispheres tested by asking pt to use objects / imitate certain movements

Types

Limb kinetic apraxia

Motor disability of onelimb, in absence of gross wkness / ataxia

Ideomotor Inability to do the command despite comprehending the command & adqt motor & sensory fntns i.e., defect in execution

Ideational apraxia

Loss of ideas behind skiled movements Pt name & describe object but not know how to manipulate it

Buccofacial apraxia

Pt cant perform learned skiled movementsof mouth, lips, tongue in absence of motor paralysis of concerened muscles

Agnosia Failure to recognize known objects in presenc of intact sensory, auditory &

visual pathway

Type Description Lesion Tactile agnosia Pt not recog objects though Rt & lt parietal operculum

sensory, motor & coordination normal

Postr. Insula

Visual agnosia Not recog object seen with eyes though visual pathway intactObj’s color, size are described

Bilat / left occipitotemporal

Propasognosia Inability to identify familiar face Parieto occipital lesionAnosognosia Lack of awareness to recog

paralysed limbRt parietal lobe lesion

f. Handedness – rt / lt g. Sleep

duration, intermittent awakening, day time sleeping (narcolepsy), sleep walking & other motor activities (somnambulism), sleep aneuresis

Disorders Dyssomnia Intrinsic Extrinsic

Psychophysiologic, idiopathic, narcolepsy Adjustment sleep disorder, altitude insomnia,food allergy insomnia

Parasomnia Arousal disorders Asso. With REM slp

Confusional arousal, sleep walkingNightmares, sleep paralysis, sleep related painful erection

Disorders asso with medical/ psychiatric disorder

Mental disorder- schizophrenia, anxiety, depressionNeurological disorder – parkinsomnism, sleep related epilepsyMedical- sleeping sickness, COPD, chronic renal failure, drugs

Somnambulism Common in children & adolescentsSleep eneuresis Primary – fsilure to attain continence since birth

Secondary – emotional disturbance, UT Infection &malformations, Epilepsy, Cauda equina lesion

Lobar functions & lesions:

Frontal Personality, emotion, social behaviourParietal Dominant lobe-language, calculation, appreciation of size, shape,

texture & weightNon-dominant lobe - spatial orientataion, construction skill

Temporal Dominant- Speech, Language, Olfaction, Varbal memory, Auditory perception

Non dominant- Muscle tone, Non- verbal memory (face, shape, music)Occipital Analysis of vision

Frontal lobe Lesions

Unilateral frontal Right/ left lobe

Contra lateral spastic HemiplegiaAnosmia [orbital part]Impaired memory

Prefrontal Presence of primitive reflexes [grasping & sucking]Elevation of mood, TalkativenessLoss of initiative

Bilat frontal Bilateral Hemiplegia, Pseudobulbar palsyPrefrontal lesion-abulia / akinetic mutism, lack of attention & problem solving ability, labile mood, Primitive reflexes

Dominant left lobe

Agraphia, Apraxia of lips & tongue, Loss of Verbal Fluency

Parietal lobe lesions

1. Unilat. Lobe Lt / Rt

Cortical sensory loss, mild hemiparesis, homonymous inferior quadrantanopia, neglect of one half of body

2. Dominant Lt lobe

In addition to defects in (1) above Disorders of Language[alexia], Gertsman’ syndrome [defect in writing, calculaton, finger agnosia, Right & left disorientation], Tactile AgnosiaBilateral Ideomotor & Ideational Apraxia

3. Non dominant Rt lobe

In addition to (1)Dressing apraxia, Anosognosia, Construction Apraxia, Visuospatial disorders

4. Bilat Visuospatial imperception, topographic memory loss, Anosognosia, Construction apraxia, Spatial disorientation

Temporal lobe lesions

1. unilat Rt / Lt Hallucinations – auditory, visual, olfactory, gustatory Emotional & behavioural changes, Dreamy state with Uncinate seizures, Homonymous superior Quadrantinopia

2. dominant Lt. lobe

In addition to (1)Alexia, Color anomia (Splenium of corpus callosum)

3. non dominant Rt. Lobe

In addition to (1)Inability to judge spatial relationships in some casesImpairment of non verbal memory Agnosia fo sounds & some qualities of music

4. bilateral a. Korsakoff amnesic defectb. Apathy & Placidityc. Increased sexual activityd. Sham rage b + c + d = Kluver Bucy syndrome

Occipital lobe lesions 1. unilat (Rt / Lt)

Contralat. Homonymous hemianopia – central/ peripheral Elementary Hallucinations in irritativee lesion

2. dominant left In addition to (1)

lobe Alexia & Color anomia (Splenium of cor. Callosum), Object agnosia 3. non dominant rt lobe

in addition to(1)Loss of visual orientation & topographic memory, Contralateral homonymous hemianopia, hallucinations

4. bilateral Cortical blindness (pupils reactive) Loss of color perception, Inability to identify familiar faces (Proposognosia)

2. Cranial nerves

Olfactory nerve

o rule out local lesion o Sense of smell in each nostril separatelyo Items used – Tea, Coffee, Astafoedia

Lesions Anosmia: loss of smell sensationCauses - nasal diseases, head injury, tumours of anterior cranial fossa, chronic basal meningitis (TB, Syphilis, Neoplasm), Kallman’s syndrome (anosmia, obesity, hypogonadism)

Optic nerve o Visual acuity – each eye separately at 6 mts;

At Bedside – Snellen’s charts

o Visual field – by confrontation method

o Colour vision – Red, Green, Blue & Yellow

o Fundus examination

Lesions 1. decreased visual acuity Primary ocular disorders, Refractory errors, Papillitis,

Retrobulbar neuritis2. unilateral loss of vision – Ocular lesions, Carotid hemiplegia 3. defects of visual field(scotoma = characteristic field defects)

Types of scotoma Name Definition Types & causesCentral Scotoma

Loss confined to Central region of

Unilateral – diseases of Choroid, multiple sclerosis

Pure motor cranial nerves 3,4,6,11,12Pure sensory cranial nerves 1,2 & 8Both motor & sensory cranial nerves

5,7,9 & 10

field of vision Bilateral (biltl) – vit B12 deficiency

Para central scotoma

Disease of Choroid / Retina near the macula

Unilat. – vascular disease like retinal embolism,

retinal artery occlusion

Bilat – toxic causes like Alcoholism, B12 diseases

Arcuate – (comma shaped) Glaucoma damaging

nerve bundle in retina / optic nerve

Concentric constriction

Concentric constriction of visual field

Long standing papilloedema, bilat. lesions of

Striate (visual) Cortex, Retinitis pigmentosa,

Hysteria

Hemianopia Loss of vision in one half of visual field

Homonymous –nasal field of one eye & temporal of otherHeteronymous – loss of nasal / temporal of both eyesBitemporal – lesion of optic chiasm (pituitary tumor), compression in mid-line Binasal – lateral compression of chiasma

Quadrantanopia Lesions of optic radiation & calcarine cortex

Superior - temporal lobe

Inferior – parietal lobe

4. papilloedema – all causes of raised intra cranial tension (tumors, abscess),

central vein occlusion, HT, Polycythemia, Toxins (vit. A

intoxication. Hypoparathyroidism)

5. primary optic atrophy –Neuro- syphilis, Sellar / Para sellar tumor,

Fredreich’s ataxia, Leber’s optic atrophy, Multiple sclerosis

6. color blindness – hereditary & bilat. Visual cortex lesions

7. pupilary reflex Afferent lesions (optic merve)

Direct reflex lost, Consensual reflex preserved

Efferent lesions (3rd nerve)

Pupil fixed & dilated – direct reflex lost, Accomodation also lost Response is seen in contra lat. Pupil

III, IV & VI nerves 1. Ocular movements

Action of ocular muscle

Lesions Diplopia (double vision)

Types – Uni & Binocular; Crossed & UncrossedUniocular Due to ocular conditions Binocular Weakness of Muscles; Occurs when Eyes are openCrossed Paralysis of ADDUCTOR Muscle - Medial, Superior & Inferior recti

palsyUncrossed Paralysis of ABDUCTOR Muscle – Lat rectus, Sup & Inf. Oblique

palsy

2. Pupil – position, size, shape, equal / unequal Pupil size (normal 3-5 mm)

Miotic <3 mm Old age, Horner’s syndrome, Pontine hemorrhage, Drugs like morphine, Neostigmine, Organo phosphate poisoning

Mydriatric >5mm 3rd nerve palsy, Optic atrophy, InfantsDrugs like Atrophine, Pethidine

Special types of pupil Definition Seen in diseases

Argyl Robertson pupil

Small, irregular, unequal. Light reflex lost Accommodation reflex preserved, Poor response to mydriatric

Neurosyphilis (tabes dorsalis), DM, encephalitis, Disseminated Sclerosis

Horner’s syndrome(Sympathetic lesion)

Miosis, Anhydrosis, Enopthalmos, Ciliospinal reflex absent

Vasculitis, encephalitis, Syringomyleia, Pan coast’s tumor, Cervical rib, Brain stem lesion, pontine glioma

Hippus Alternate rhythmic dilatation & contraction of pupil

Multiple sclerosis, Syphilis, Neoplasm

Elevators Sup rectus, Inf obliqueDepressors Inf rectus, Sup obliqueAbductors Lat rectus, Inf obliqueAdductors Med rectus, Inf obliqueInternal rotators (intorsion ) Sup rectus, Sup obliqueExternal rotators (extorsion) Inf rectus, Inf oblique

3. Reaction of light – direct & consensual4. Accommodation & ciliospinal reflex5. Nystagmus – vertical / horizontal / rotatory

Definition - Involuntary, Conjugate, Rhythmic oscillations of Eye. Normally occurs on extreme gaze, lasting for 10 secs

Types- Pendular & Jerky

Definition Causes Pendular Rapid horizontal oscillations to either

side of midline, of Equal amplitude,Seen on forward gaze

Visual defects from Infancy – Macular abnormalities, Chorioretinitis, Albinism, High infantile myopia, Opacities in the media, Retinitis pigmentosa

Jerky Occular oscillations of Unequal amplitude with slow drift in 1 direction & fast correcting movement in the other, fast phase determining the direction of Nystagmus

Refer below

Types & cause of Jerky Nystagmus:1. Horizontal To & fro movement

of eye ball in horizontal plane

Lesions of Vestibular nerve& nuclei, Medial longitudinal bundle, Cerebellum [Nystagmus to the side of lesion]

2. Vertical Up & down movement of eye ball in vertical plane

Seen in conditions involving Brain stem – Vascular accident, Encephalitis, Multiple sclerosis, Syringobulbia, druds [ anticonvulsants, BZD, Barbiturates], Wernicke’s encephalopathy

3. Rotatory Osscilatory movement of eye ball whch is rotatory in character

Seen in Labyrinthine disorders

Rare forms of Nystagmus: See saw nystagmusConvergence retraction nystagmusUpbeat nystagmusDownbeat nystagmusRebound nystamus

6. Ptosis narrowing of palpebral fissure) Partial / complete, uni / bilateral

Bilateral Myasthenia gravis, Myopathy, Bilat. Horner’s, Snake bite, Botulism

Lesions of 3rd nerve inMid brain (levator palpebra superioris involvement)

Unilateral Pea aneurysm, Herniation of uncus, Cavernous sinus thrombosis, DM, HT, Collagen disease, Horner’s syndrome, Trauma 3rd nerve palsy with papillary sparing

Congenital Ptosis due to Aplasia of 3rd nerve nuclei

Trigeminal nerve Motor – temporalis, masseter, PterygoidsSensory – sensations over the faceCorneal & conjunctival reflex

LesionsName Affected area Diseases

Nuclear lesion Diseases affecting Pons, Medulla, Upper cervical cord(C2)

Tumor, Demylination, Vascular lesions, Syringomylia / Syringobulbia

Preganglionic nerve lesion

Preganglionic Assiociated lesions of other cranial nerves esp VI, VII, VIII

Tumors (Meningoma, Nasopharyngeal carcinoma, Cerebello-pontine angle tumor), Meningeal irritation (Acute / chronic meningitis, Carcinomatus meningitis)

Gasserian ganglion lesions

(Characterised by severe facial pain)

Tumors, Abscess, Herpes-zoster opthalmicus

Post ganglionic lesions

- a. Cavernous sinus lesionb. Gradenigo’s syndromec. Superior orbital fissure syndrome

Facial nerve Motor: eye- Frowning, eye closure, Raising of Eye brows, Browing,

Mouth & cheek – whistle, showing teeth, nasolabial fold, platysmaSensory: taste in antr 2/3 of tongue

LesionsTypes – unilat. & bilat.; each being futher divided as upper motor neuron type (UMN) & lower motor neuron type(LMN)

Lesions Causes Unilateral

UMNLMN

Usually vascular, Cerebral tumor, Multiple SclerosisBell’ s palsy, Parotid tumor, Head injury, Skull base tumors, DM, HT

Bilateral UMNLMN

Vascular, Motor neuron diseaseGuilian – barre Syndrome (GBS), Sarcoidosis – Uveoparotid

Fever, Leprosy, Leukemia, Lymphoma

Differences between UMN & LMN type of facial palsy

Bell’s phenomenon (movement of eye ball upwards & inwards on closing eyelids- well seen)

Bell’s phenomenon absent

Emotional fibres spared Emotional fibres involovedAssociated with Long Tract signs Absent Exaggerated Jawjerk Normal Jaw Jerk Corneal reflex present Absent

Vestibulocochlear nerve

Acuity of hearing (eg- rubbing of paper) in both ears separately

Rinne’s test: using tuning fork ( 256 or 512hz) over mastoid process & then lateral to ear & find out when it is louder.

Positive Air > Bone

Normal ear Nerve deafness(sensorineural deafness)

Negative Bone > Air

Middle ear deafness (conductive Deafness)

Weber’s test: place vibrating tuning fork over middle of fore head,

Point of Application (middle of forehead)(No lateralization)

Normal

Better in Normal Ear (lateralized to normal side)

Nerve deafness on Opposite side

Better heard in Affected Ear (lateralized to affected side)

Conductive deafness on Same side

Lesions of VIII nerveVertigo = hallucinations of movement of either the body / the surroundings

causes – peripheral labyrinthine disorders, Cerebellar lesions, VBI

Deafness – neural Peripheral labyrinthine disorders – Acoustic neuroma, Meniere’ s disease, Vestibular neuronitis

IX & X neves [glossopharyngeal & vagus]: Gag reflex & say ‘ah’ & look for deviation in uvulaSensations in posterior 1/3rd of tongue & pharynx

Lesions of IX, X, XI nerves

Bilateral Palate remains immobile on both sidesDysphagia, Nasal regurgitation,Pharyngeal reflex absent

GBS, Polyneuritis, Myasthenia gravis, Motor neuron Disease

Unilateral Palatal arch on that side is at lower level than on healthy side

PICA, Tumor, Demylination, Syringobulbia, Secondaries, meningioma, Stroke

Accessory nerve Trapezius & sternomastoid – shrugging of shoulder with & without resistance, turning head on both sides separately with & without resistance

Hypoglossal nerve Appearance of tongue, wasting / contracted/ FasciculationsMovement of tongue & deviation of tongue

Lesions of XII nerve

Causes – infarction, tumour, MND, VB aneurysm, trauma, meningioma, metastasis

Types – LMN & UMN

Differences between LMN & UMN of XII nerve Wasting Present AbsentFibrillation Present Absent Tongue

Tone Deviation Protrusion

Flaccid Towards affected side Possible

Small & spastic - Difficult

Jaw jerk Normal Exaggerated

3. Motor system:a. Nutrition (bulk of muscle)

i. comparing with Opposite side, palpating the musclesii. Note any wasting / hypertrophy & its distribution-

predominantly Proximal / Distal / Both Feel for muscles

Atrophic muscle FlabbyHypertrophic muscle

Firm / Rubbery

iii. Measure the circumference of limbs

Lesions Hypertrophy – physiological / pathological

Muscle wasting 1. generalized 2. upper limbs

i. predominant Proximal muscle

Spinal muscular disease, Motor neuron disease, Syringomyelia, Compressive lesion (C5- C6), Lesion of upper brachial plexus (Br Plxs) like Erb’s paralysis, late stage of muscular dystrophies, inflammatory disease (poliomyelitis, Poliomyositis)Motor neuron disease, syringomyelia, Cervical cord tumors

ii. Predominant Distal muscle

(C8,T1), lesion of lower Br. Plxs (Klumpke’s paralysis), cervical rib, cervical gland enlargement, Pancoast syndrome, traumatic lesion of Radial, Median, Ulnar nerves, peripheral neuropathy, Peroneal muscular atrophy

iii. small muscle of hand

Vertebral lesion (metastasis), spinal cord lesions (syringomyelia, tumors), antr. Horn cells (motor neuron disease, poliomyelitis), root lesions, br. Plxs (klumpke’s paralysis, cervical rib), peripheral nerve lesion (hansen’s disease, Carpal tunnel syndrome), disuse atrophy (fracture plaster)

3. lower limbs

Only Lower limbs Cauda equina lesion, Peripheral neuropathy, peroneal muscular atrophy, poliomyelitis, peripheral nerve trauma (lat. Popliteal nerve), tarsal tinnel syndrome

Upper limbs in addition LL

Peroneal muscular atropy, Chronic poly neuropathy, Spinal muscular atrophy, Hansen’s disease

b. Tone (degree of tension present in a muscle at rest )Normal / hypertonia / hypotonia

Hypertonia- resistance on passive movement Spastic / rigid

Spasticity RigidityDefinition State of hypertonia in which

tone in antigravity muscle groups > muscles assisted by

State of hypertonia in which tone in antigravity muscle groups = muscles assisted by

Upper limbsArm Forearm

1. 10cm Above Olecranon2. 10 cm Below Olecranon

Lower limbsThigh Leg

1. 18cm Above patella 2. 10cm below Tibial

tuberosity

gravity gravityDiseases Pyramidal lesion (UMN) Extra pyramidal lesion

Types of rigidity Plastic / lead pipe rigidity

Uniform resistance offered to passive movement

1. Parkinsonism (post encephalitic)

2. basal ganglia neoplasms

3. catatonia Cog wheel rigidity

Resistance offered to passive mvmt interrupted by alternate contractions of agonist & antagonist muscle due to Asso. Tremor

1. parkinson’s disease 2. over dose of reserpine,

Chlorpromazine3. carbon monoxide

poisoning

Causes of hypotonia i. lesions of motor side of Reflex arc - Poliomyelitis, Polyneuritis, trauma of peph.

nerveii. lesions of sensory side of “ “ - Tabes dorsalis, herpes zoster, carcinomatous

neuropathiesiii. combined motor & sensory lesions – syringomyelia, cord / root compressioniv. cerebellar lesions, Chorea

Clonus Sudden stretching of muscle produces reflex contraction. If stretch maintained during subsequent contraction further reflex contraction occurs & continues till stimulus removedDorsiflexion of the foot after flexing the hip & knee ( ankle clonus), sharp movement of patella downwards ( knee clonus)Sustained clonus => pyramidal tract lesion (UMN)Illsustained => tense persons, after straining (defecation)

c. Power Tested in all joints (flexion, extension, abduction, adduction) Grading (Medical Research Council)

Grade 0 No visible contractionGrade1 Visible musle contraction, but no movement of jointsGrade 2 Movement with gravity eliminatedGrade3 Movement against gravityGrade 4 Movement against resistanceGrade 5 Normal power

d. Coordination

upper limb 1. Outstretched arms test 2. Finger Nose test 3. Nose – Finger Nose test 4. Finger to Finger test5. Pronation –Supination test6. Pointing & Past pointing test

4. lower limb i. Finger Toe testii. Heel – Knee test iii. Tandem walking

e. Involuntary movements

Name Definition Causes & types Chorea semi-purposive, irregular,

non- repetitive &brief jerky movement arising in proximal joints & appearin g to flit from one part to other randomlyIncreased on attempting voluntary movement & Exacerbated by emotional disturbance

Lesion in caudate nucleus Genetic – huntington’s, hereditaryHemichorea – stroke, tumor, trauma, post thalamectomyDrug – neuroleptics, phenytoin, alcohol, oral contraceptivesSymptomatic chorea – Encephalitis lethargica, sub dural hematoma, Cerebrovascular disease, hypoparathyroidism, hypernatremia , primary polycythemia

Athetosis Slow writhing movement Best seen at wrists (flexing), fingers (writhing), foot (inverted)

Lesion in putamen

Hemiballismus

Proximal joints of one arm resulting in Wild, Rapid, Flinging movement of wide radius, occurring constantly with short periods of freedom

Lesion in subthalamic nucleusMost dramatic of all involuntary movements – may injure patient / bystanders

Dystonia Involuntary sustained muscle contractions frequently causing Twisting & repetitive movements

Genetic – primary generalized D, Focal adult onset DHeredito degenerative – Ataxia telangectasia, Lipid storage diseases, Wilson’s diseases, Parkinson’s diseaseSymptomatic – Athetoid cerebral palsy, cerebral anoxia, post-encephalitic dystoniaDrugs – neuroleptics, Mn poisoning,

LevodopaHemidystonia – stroke, trauma, tumor, AV malformations

Tremors Rhythmical & oscillatory movement of body part caused by rhythmic contractions of agonst & antagonist muscles

Rest tremors – parkinson’s disease, post encephalitic parkinsonism, drug induced parkinsonismPostural - physiological, thyrotoxicosis, anxiety, alcohol, caffeineIntentional – lesions of cerebellum & its connections in diseases like multiple sclerosis, Spinocerebellar degeneration, tumor

Myoclonus Rapid, brief shock like muscle jerks that are often repetitive & rhythmical

Generalized – progressive myoclonic encephalopathies, hereditary myoclonus, metabolic (Tay- sach’s & Batten’s disease), Alzheimer’s diseaseMetabolic – Uremia, hyponatremia, hypocalcemia, hepatic failureDrug induced, alcohol & drug withdsnalFocal / segmental – spinal tumor/ infarct/ trauma, palatal myoclonus

Tics Repetitive, irregular stereotyped movements / vocalizations that can be imitated,

Simple tics – transient tic of childhood, chronic simple ticComplex multiple tics – chronic multiple ticsSymptomatic tic – encephalitis lethargica, drug induced, post traumatic

Fasciculatn Irregular, non rhythmic contraction of muscle fascicles

Motor neuron disease, syringomyelia, cervical spondylosis, peroneal muscular atrophy, poliomyelitis (in recovery stage)

Fibrillation Contraction of individual muscles

Denervation hypersensitivity Easily perceived over the tongue where they are easily seen under mucus membrane

Titubation Involuntary nodding of head Lesions of Vermis of cerebellum

f. Gait Patient is asked to walk in a straight line for at least 9 metres, & asked to turn and walk back

Gait Seen in Description Circumduction gait

Hemiparesis Pt. throws his lower limb outwards at hip joint (circumduction), & leans towards opposite healthy sideAffected arm adducted at shoulder & flexed at elbow, wrist & fingers

Spastic gait Lesion of UMN involving both lower limbs

Adductor spasm causes legs to cross each other & each foot trips the other

Scissors gait Marked spastic gait as in cerebral diplegia

Marked spasm of adductors of lower limbs

High stepping gait

Pts with foot drop Pt raises foot high to overcome foot drop & on keeping foot down toe hits ground firstThere is no ataxia

High stepping & stamping gait

Posterior column lesion (gross loss of position sense)

Pt not know where his foot is & so on walking raises foot high up in air & brings it down forcefully (stamping gait), heel touches ground firstMore prominent in dark / pts ‘ eyes closed

Ataxic gait Cerebellar lesion Pt is ataxic & reels in any direction including backwards & walks on a broad baseDifficulty in tandem walking

Shuffling gait Extra pyramidal lesionAssociated with rigidity esp. Parkinsonism

Series of small flat footed shufflesParkinsonism – pt. stooped posture (universal flexion) & walks in small, shuffling steps as if trying to catch up with center of gravityAutomatic assoc. upper limb absent

Waddling gait

Primary muscular disease- proximal weakness of lower limbs(muscular dystrophy)/ bilateral hip problem (congenital dislocation of hips)

Pt walks with broad base with exaggerated lumbar lordosis

Lesions of Extra pyramidal system

Sign Site of lesion Resting tremor Substantia Nigra, Red nucleusMuscular rigidity SN, PutamenHypokinesia SN, Putamen, Globus pallidusChorea Caudate nucleus Hemiballismus Sub – thalamic nucleusDystonia, Athetosis Putamen

Signs & symptoms of Parkinson’s disease & Parkinson plus syndrome (progressive

supranuclear palsy, Dementia with Lewy bodies, Multiple system atrophy)

Feature Parkinson’s disease Parkinson plus syndrome Tremor Rest tremor (pill rolling) Action tremor & impotence Tone Rigidity -cogwheel (best seen in

UL) / lead pipe(best seen in LL & trunk)

Marked axial rigidity

Movements Bradykinesia -Thought process Bradyphrenia (slow thought) -Saccades & Slight jerky saccades Vertical supranuclear

pursuit movements

Pursuit eye movements saccade (PSP)Broken pursuit (MSA)

Facial expressions

Facial hypomimia (lack of facial expression)

-

Handwriting Micrographia (small hand writing)

-

Posture Gait

Stooped Festinant (short shuffling gait)

Falls early in disease courseAtaxic

ANS dysfunction

Mild Severe

4. Sensory system : i. Spinothalamic sensations

a. Touch Skin is lightly touched with Cotton wool shaped to a point

with eyes open & closed in dermatomal areas b. Pain Superficial pain - Sharp pin is used

Deep pain – squeezing of muscles (usually of calf) & tendons

c. Temperature Hot & cold water

Sensory levels (spinal cord shorter; end at L1)

Vertebrae Segmental level of spinal cordLower cervical +1T1-6 +2T7 -9 +3T10 Overlies L1 & 2T11 “ L3 & 4T12 “ L5L1 “ sacral & coccygeal segments

ii. Posterior column sensations a. Vibration sense

128 hz preferred over 512 hz as 128 hz fork decays later Only stem of fork touched (not the pongs) on bony

prominences b. Joint sense

Eyes closed Joint fixed & digit moved up / down Ask pt. to tell direction of movement Repeated many times avoid alternate movements

In posterior column deficit there is numbness in affected limb

c. Position sense Pt’s eyes closed & ask pt to Tip of Forefinger of one hand with other Place forefinger on tip of nose & heel on knee

accurately d. Romberg’s sign

Pt stands upright with feet together & eyes closed In proprioceptive / vestibular deficit balance is impaired & pt

may fall if not caught Minimal lesions demonstrated by asking to stand on toe with

eyes closed e. Lhermette’s sign / barber chair sign

In lesion of postr column of cervical region sudden flexion / extension of neck give rise to Electric shock like sensation that travls rapidly down trunk & even hands, feet

+ ve in Multiple sclerosis, Cervical spondylosis, Syringomyelia, tumor of cervical cord, Subacute combined degeneration of spinal cord

iii. Cortical sensations1. Tactile localization

Ability to correctly localize pt. touched with head of pin / finger tip

2. Tactile discriminationFinger pulp & lips 3-5 mm well

recog.Palm 2-3 cmSole 4 cmDorsum of foot, Legs, Back

> 5 cm

Loss of Tactile Discrimination in presence of intact Posterior Column sensation => Parietal lobe lesion

3. Stereognosis Ability to identify object purely by feel of its

shape & size Use familiar objects

4. Barognosis 5. Graphesthesia

Ability to recognize letters/ numbers / diagrams written on skin with blunt point

Loss of graphaesthesia (agraphaesthesia) – seen in lesions of parietal lobe when peripheral sensations are normal

6. Cortical inattention

Various Sensory signs & Lesions

Tot Contralat loss of all sensation

extensive lesion of thalamus, usually vascular

Contralat loss of only Exteroceptive sensatn

Partial lesion of thalamus, Lesion in lat. Part of brain

stem

Contralat loss of only Proprioceptive sense

partial lesion of thalamus, lesion in medial part of brain

stem

Contralat loss of Position sense

& Cortical sensatn +

disturbance of light touch &

pain

parietal lobe lesion / lesion between thalamus & cortex

contralat Hyperalgesia &

Hyperesthesia

partial lesion of thalamus

Loss of Pain & Temp on Same

side of Face & Opp. Side of

body

Lesion of medulla affecting descending root of V nerve &

asc. Spinothalamic tract of rest from rest of the body

Unilat. Loss of pain & temp

below definite level

Brown Sequard syndrome

Glove & Stocking anaesthesia,

(all sensation lost over a clearly

defined part of body like area of

glove & stoking)

lesion of peripheral nerve / sensory root as in diabetes

mellitus, polyneuropathy, mononeuritis multiplex

Patchy area of sensory loss chronic polyneuritis, Leprosy, tabes dorsali mononeuritis

multiplex

loss of sensation of Saddle type impairment of sensation over lowest sacral

segm. it affects all forms of sensations accompanied by

loss of leg reflexes & sphincter control indicates major

lesion of cauda equina

if touch is preserved => lesion near conus in which

plantar reflexes may be extensor & knee jerk may be

retained

loss of Vibration sense alone if affecting lower limbs =>intrinsic cord lesions like

multiple sclerosis, syringomyelia

loss of Position & Vibration

only

postr. Column lesion as in tabes dorsalis,

subacute combined degeneration

5. Reflxes:i. Superficial reflexes

Reflex Technique Segm. Innervation Normal resultCorneal Corneal edge with cotton

wisp, Pt look in opp. Direction

Afferent – V nerve Center – pons Efferent – VII nerve

Brisk closure of eyes

Conjunctival Bulbar conj. With wisp of cotton

-do- -do-

Pharyngeal Posterior pharyngeal wall tickled

Aff – IX nerve Cen – medulla Eff – X nerve

Contraction of pharyngeal muscles

Palatal Soft palate tickled Aff –V nerve Cen – medullaEff – X

Soft palate moves up

Scapular Stroke skin in inter- scapular area

Aff – C4-5Cen – C4-5Eff – dorsal scapular nerve

Contraction of scapular muscles

Abdominal Abd. Wall lightly stroked from without inwards, all 4 quadrants

Upper abd: T7- T9Mid :T9- 10Lower: T11,12

Muscles in quadrant stimulated contract & umbilicus moves in that direction

Cremasteric Upper & inner part of thigh stroked downward & inward direction

Aff – femoral nerve Seg – L1,2 Eff – genitofemoral nerve

Contraction of cremasteric muscle puls up scrotum & testicle on that side

Plantar Pt’s thigh externl rotated, Knee slight flexed, Ankle fixed with hold of examiner, outer sole stroked with blunt key, then forward, & inward along

Aff – tibial nerve Seg – L5, S1,2Eff – tibial nerve

Big toe flex at metatarsophalangeal jt. & flexion of other toes Babinski’s sign –extension of big toe with extension & faning out of other toes

metatarsophalangeal joints

Clinical Significance of Babinski’s sign 1. Lesions of corticospinal tract (pyramidal tract)2. infancy ( upto 1year)3. deep sleep 4. deep anesthesia5. narcotic overdose 6. alcohol intoxication7. post traumatic state

Other methods of eliciting Plantar reflexes 1. Oppenheim reflex – firm stroke with finger & thumb down either side of antr,

brdr. Of tibia , more pressure on mdl side2. Gordon reflex – calf muscles squeezed3. Chaddock reflex – light stroke below lat. malleolous

ii. deep reflexes Spinal segment involved

Biceps C5Triceps C7Supinator C5, 6Hoffman C7, 8, T1Knee L3, 4 Ankles L5, S1Pectoral C7Deltoid C5

All reflexes should be tested on both sides Grading

iii. Inverted reflexes

Reflex Procedure Lesion Inverted radial reflex

Supinator jerk => absence of elbow flexion but there is finger flexionBiceps jerk absent & triceps exaggerated

Presence => C5,6 segment lesion

Inverted biceps

Biceps reflex => no flexion of elbow but extension of elbow due to triceps contraction

Presence=>C5,6 segment lesion

Inverted Knee reflex

Knee jerk => no extension instead flexion of knee due to contraction of

Presence=>Lesion of L2,3,4

0 Absent 1 Present as Normal jerk 2 Brisk as a normal Knee jerk3 Very brisk 4 Clonus

hamstrings

iv. Other allied reflexes

Reflex Procedure Lesion

Hoffmann reflex

Terminal phalanx of pt’s mid finger flicked downwards between examiner’s finger & thumb

In hypertonia tips of other fingers flex & thumb flexes and adducts

Wartenberg’s reflex

Pt’shand supinated, slightly flexing fingers with thumb in adduction , Examiner pronates his hand & links his hand with that of pt’s fingers. Both flex their fingers & pull against each other’s resistance

Normally thumb extends but terminal phalanx may flex slightlyIn hypertonia => thumb adducts & flexes stronglyIndicating pyramidal tract lesion

v. sphincteric reflexes ask the pt. for difficulties in Swallowing, Defecation, Miicturition, Sexual function

vi. primitive reflexes (released reflexes) Deficit of frontal function release primitive motor behavior which

includes following reflexes

Reflex Description Clinical inference Pout reflex

Rubbing of chin causes pouting / “sucking” lip movements

Polysynaptic reflex released by frontal lobe disease / diffuse degenerative brain disease

Grasp

reflex

Pt tends to grasp objects esp

examiner’s fingers when they are

placed in his palm, esp in contact

between thumb & index finger

-

Palmomental reflex

Scratching the palm produces unilateral contraction of mentalis muscle

Non specific sign sometimes seen in normal people also

6. Autonomic nervous systemi. check pupillary response to light & accommodation

ii. skin –dryness => absence of sweating iii. resting tachycardia- present / not iv. pulse rate slowing with deep inspirationv. trophic changes in distal skin – absence of hair growth, nail

bed

Bladder InnervationInnervation Segment Part innervated Parasymp. Emptying

S2,3,4 Detrussor muscle via pelvic nerve

Symp. (also carries pain sensation ) – filling

T11, 12, L1,2 Trigone muscle via presacral & hypogastric nerves

Somatic S2,3,4 External sphincter & perineal muscle pudendal nerve

Types of Bladder & Levels of Lesions, clinical condition Incomplete spastic / uninhibited bladder

Post central – loss of awareness of bladder fullness, incontinencePrecentral – difficulty in initiating micturitionFrontal – inappropriate micturition, loss of social control (like infant’s bladder)

Complete spastic / reflex / automatic / hypertonic bladder

Lesion in spinal segments above S2,3,4

Autonomous bladder / hypotonic

Lesion at S2,3,4 & Cauda equina

Sensory paralytic (afferent pathway lesion )

Seen in DM, Syringomyelia, Tabes dorsalisIntact voluntary initiation of micturitionUrinary retention- overflow incontinenceFrequent urinary tract infection

Atonic bladder (reflec arc lesion)

Seen in Tabes dorsalis, Conus & Cauda

Motor paralytic (efferent pathway lesion )

Seen in lumbar canal stenosisLumbo-sacral meningio- myelocelePainful urinary retention

7. Cerebellar signs Parts

Lesions of cerebellum Clinical signs

1. Hypotonia , 2. Dysmetria (inappropriate range of movement)3. Intention tremor 4. Adiadochokinesia 5. Rebound phenomenon6. Nystagmus – quick & towards direction of gaze, occasionally skew

deviation in acute lesions

Part Connected to Function Archicerebellum Vestibular nuclei Maintain equilibriumPaleocerebellum Spinal cord Maintain posture Neocerebellum Cerebral cortex Center of voluntary movements

7. Jerky, explosive speech, Disturbance of articulation & phonation in lesion of vermis

8. Gait – staggering towards affected side + ataxia 9. Pendular knee jerk 10. Titubation

Causes1. Fredreich’s ataxia (other signs – scoliosis, pes cavus, Ataxia, Dysarthria,

Nystagmus, Muscle weakness, Optic atrophy, Deafness)2. Cerebellar abscess (acute) & tumors, paraneoplastic syndrome 3. Vascular causes 4. Hypothyroidism 5. Alcohol6. Drugs like Phenytoin, Babiturates, Aminoglycosides 7. Refsum’s disease

8. spine & cranium a. Anomalies

i. Gibbus = localized angular deformity caused by fracture, pott’s

disease, TB, Metastatic malignant deposit

ii. Lordosis = increased backward bending of spine

Increased cervical lordosis

Ankylosing spondylitis

Loss of cervical laordosis

Acute lesions, rheumatoid arthritis, cervical spondylosis

Increased lumbar lordosis

Muscular dystrophies

Loss of lumbar lordosis

Acute disc collapse, aging, ankylosing spondylitis

iii. Scoliosis = lateral curvature of spinePostural, congenital, unequal limb in length, acute disc collapse,

Extensive fibrosis of lungs, inflammatory disorders

iv. Kyphoscoliosis = lateral + posterior bending of spine (kypho = backward bending)

Congenital, poliomyelitis, neuromuscular disordersv. Tenderness

vi. Height- neck ratiovii. Auscultation over skull

b . Signs of meningeal irritation

Usually meningitis, sub-arachnoid hemorrhage

Sign Procedure Normal In Meningeal irritation

i.stiffness

Passively but gently flex pt’s neck

chin touch chest without pain

Flexion causes Pain in posterior part of neck & Movement is resisted by spasm of extensor muscles

ii.sign

Pt supine on bed Passively extend pt’s knee on either side when hip is fully flexed

no pain / spasm (this test is less sensitive than neck stiffness)

Pain & Spasm of hamstrings in Meningeal irritation of lower part of spinal sub-arachnoid space

iii. Brudzinki’s sign iv. Ophisthotonus

9. OTHER SYSTEMS CVS

Look for Hypertension, valvular heart disease, [AF] TOF, Peripheral pulsation, carotid pulse & bruit

RS:Look for

Evidence of TB, lung abcess, bronchiectiasis, corpulmonale, bronchogenic carcinoma

ABDOMEN:Look for

Hepato-spleenomegaly, ascitis, polycystic diseases, hepatocellular failure, any mass

Blood supply of CNSBlood supply of cerebrum

Artery Area supplied Lesions Anterior cerebral artery

Entire Mdl surface + 2 cm strip along Superolat surface & Mdl ½ of Orbital surface

Hubner’s branch (antr int capsule) => faciobrachial monoplegiaMain trunk=> Contralat leg, micturirtion & cognition affected

Middle cerebral artery

Entire Ltl surface + Lat ½ of orbital surfaceSuperior divisison - broca’s area Inferior division - Wernick’s area

Lenticulo-striate (LS) branch [int capsule - superior half] , Medial & lat striate branches (corpus striatum)Occlusion of LS vessels =>hemiparesis without cognitive defect & no sensory lossTerminal branch => hemiparesis affecting face & armMain trunk => combination of above

Posterior Mdl surface of Temp Terminal occlusion=>visual cortex

cerebral artery

& Occp lobes & their Tentorial surface, Cerebellum, Medulla, Pons, Midbrain, Thalamus, Sub thalamus

Thalamogeniculate branch=> various thalamic & capsular features like hemianopia, Speech arrest, tremor, dystonia, contralat sensory loss

Main trunk=> all above effects

Vertebral artery branches a. Meningeal b. posterior, c. spinal, d. anterior spinal e. medularyf. postereior inferior cerbellar

Infarction of posterior inferior cerebellar artery

Basilar artery branches

1. Pontine artery 2. Labyrinthine artery3. anterior inferior Cerebellar artery

Infarction of anterior inferior cerebellar artery

Infarct Level Regions involved Clinical Effects

Infarct Level Regions involved Clinical Effects Paramedian infarct

12th nerve nucl, mdl lemniscus & medullary pyramid

tongue weakness, paralysis& absent uni/bi lat position sense

Basillary infarct

infr olive & pyramid Contralat ataxia & motor adaptation failure and contralat hemiplegia

Posterolat infarct (wallenberg’ s syndrome)

Symp. Tract, spinothalamic tract, nuc of tract of 5th nerve, lower vestibular nuc, infr cerbellar peduncle, 9th & 10th nerve nuclei

Ipsilat horner’s, facial numbness & ataxia, loss of contralat pinprick sensation & vestibular disturbance, speech & swallowing difficulty

Paramedian infarct

6th & 7th nerve nuclei & mdl lemniscal tract

Lat gaze failure , LMN facial wekness & loss of contra lat body position sense

Basillary infarct

6th & 7th nerve fascicles & pyramidal pathways

Diplopia, LMN facial weakness & contralat UMN facial weakness

Posterolat infarct

Symp. Pathway , Spinothalamic tract, middle cerebellar peduncle, 5th nerve nucleus, vestibular, cochlear & eye movemt control nuclei

Ipsilat sensory loss in face Ipsilat clumsiness of body & loss of contralat pin prick sensation, Nystagmus & horner’s syndrome

4. superior Cerebellar artery Infarction of superior cerebellar artery

Infarct Level Regions involved Clinical Effects Paramedian infarct

Red nucleus & 3rd nerve nucleus

Contralat ataxia & 3rd nerve palsy

Basillary infarct (weber’s syndrome)

3rd nerve fascicule & cerebral peduncle

Ipsilat 3rd nerve palsy & contralat hemiplegia (face & body)

Posterolat infarct Spinothalamic, Mdl lemniscus, & symp. Tracts & superior cerebellar peduncle

Total contralat sensory loss, ipsilat hoirner’s syndrome& sometimes ipsilat ataxia

5. posterior cerebral arteryStroke

Definition – acute neurological injury occurring due to vascular pathological processes that manifest as brain infarct /hemorrhage

Major causes Age, Obesity, HT, Smoking, DM, Alcohol, Oral contraceptives Hematological causes Polycythemia, thrombocytopenia, Sickle cell disease, leukemia, prorein C & S

deficiency Cardiac causes Rheumatic valve disease, atrial fibrillation , myocardial infarction, cardiomyopathy,

patent foramen ovale Unusual causes Marfan’s syndrome, AIDS, cervical irradiation, drug abuse, scleroderma

Clinical classification

1. completed stroke Rapid onsetPersistent ND that does not progress beyond 96 hours

2. evolving stroke Gradual step wise development of ND

3. transaient ischemic Focal ND resolves completely within 24 hours

attack4. Reversible Ischemic Neurological Deficit (RIND)

The ND completely resolves within 1- 3 weeks

Blood supply of Internal capsule

5. Superior half by lenticulostriate , branch of MCA

6. Inferior half – anteriorly ACA (Hubner’s artery),

7. Posterior limb

8. Anterior 1/3 posterior communicating

9. Posterior 2/3 anterior choroidal artery

10. ACA supplies bladder & leg areas

Blood supply of spinal cord 11. Anterior 2/3rd of cord - one anterior spinal artery

12. Posterior 2/3rd of cord - a pair of posterior spinal artery

Spinal cord Relationship of spinal segments

Vertebrae Segmental level of spinal cordLower cervical +1T1-6 +2T7 -9 +3T10 Overlies L1 & 2T11 “ L3 & 4T12 “ L5L1 “ sacral & coccygeal segments

Position of fibres Column Position of Fibres Posterior column

Fibres from Lower Limb are placed medially near central canal & from Upper Limb are placed laterally

Lateral & Anterior Column

Corticospinal & Spinothalamic tracts

Arrangement of fibres Anterior to postr (central canal to dorsum)

Touch , Position, movement, Vibration & pressure sense

Medial to lateral Cervical, thoracic, lumbar, sacral

Lesions

o Localization of segmental levelOrder of importance

First note Segmental symptoms like root pain, hyperalgesia, atrophic paralysis

Next is upper limit of sensory loss –upper limit of area of analgesia indicates lower segment compressed

Remember that “sensory level” for pain sensation suggest that, lesion is several segments lower than actual site

Segment signs Foramen magnum 1. Atrophy of sterno mastoid muscle

2. Downbeat Nystagmus

3. C2 sensory loss & cerebellar signs

4. Horner’s syndrome

5. Lower cranial nerve palsy

Cervicomedullary

junction (hemiplegia

cruciata)

Paralysis of ipsilateral lower limb & contralateral UL

(due to arm fibress ccrossing before the leg fibres at

lower part of medulla)

C2 segment 1. Sub-occipital pain / sensory loss2. Descending tract of Vnerve (pain & temp. loss

over face3. Exaggerated trapezius reflex

C3 Loss of trapezius reflex

C5 1. Inverted biceps jerk2. Inverted brachioradialis jerk (supinator jerk)3. Sensory loss over deltoid

C6 1. Dimished biceps & supinator reflex 2. Exaggerated finger flexor reflex

C7 1. Paresis of flexors & extensors of wrist & fingers2. Preservation of biceps & supinator reflex3. Exaggerated finger flexor reflex4. Inverted triceps reflex

C8 & T1 1. Weakness & wasting of small muscles of hand 2. UMN signs in lower limb3. Uni / bilat. Horner’s syndrome

Thoracic segments 1. Girdle pain / paraesthesia2. Segmental LMN involvement 3. ANS dysfunction

T3 Sensory impairment in axilla

T4 Sensory impairment below level of nipple

T6 Abdominal reflex impaired

T10 + ve beevor’s sign (intact upper abd reflex & absent

lower abd. Reflex with pull of umbilicus >3 cm on raising

the head)

T12 1. Abdominal reflex preserved

2. Sensory loss in LL staring from level of groin3. Brisk ankle & knee jerk 4. Absence of cremasteric reflex

L3, L4 1. Hip flexion preserved 2. Atrophic paralysis of quadriceps & adductors of

hip 3. Loss of knee jerk & ankle jerk

S!, S2 1. Atrophic paralysis of intrinsic muscles of foot, calf muscles

2. Knee jerk preserved3. Ankle jerk & plantar reflex lost 4. Anal & bulbocavernous preserved

S3, S4 1. Saddle anesthesia2. Bladder & bowel involved 3. Normal reflexes in LL

Compression of spinal cord

Effects of compression Slow spinal compression affects

First the pyramidal tractNext posterior column Spinothalamic tract

LMN signs

Anterior horn cell LMN signs (weakness, wasting, fasciculation)Posterior root Root pain/ girdle pain (trunk)Posterior column Lhermitte’s sign (unpleasant / electric sensation)

Constriction band around trunkPyramidal tract UMN signs

Differentiating between 1. Intra-medullary & Extra medullary lesions

Motor UMN signs Spasticity & muscle spasm

LMN signs Muscle atrophy

Trohic changes Fasciculation

Common & persistent

1or 2 segments at site of root compressionNot common Rare

Less common

Wide due to antr. Horn involvement Present Common

Sensory Root pain ……………….Funicular ………………..Dys& paraesthesias………Dissociated sensory loss….Sacral sensation………….

Joint position sense ……….Lhermitte’s sign ………….

Common Not present RareAbsent Lost

Lost Present

Rare Present Common Present Sacral sparing for Pain & TempSpared Absent

ANS Bowel & bladder disturbance Late EarlyInvestigation

X-ray of spine ……………Effect of lumbar puncture ….

Bony changes seen Signs & symptoms are pptd / increased

Not seen No such effect

2. Extra-dural & Intra dural lesion Mode of onset Asymmetrical Symmetrical Vertebral pain (local tenderness)

Uncommon Common

3. Lesions of Conus medullaris Cauda equina Onset Symmetrical Asymmetrical Disso. Sensory loss Present Absent Root pain Rare Common Fasciculation Rare Common Decubitus ulcer Rare Common Bladder & bowel Early Early / late depending

on root involvement

4. Lesions of Conus medullaris & EpiconusBladder involvement

Distension -

Faecal incontinence

Present Absent

Saddle anesthesia Present Absent Motor symptoms Absent Paralysis of LL

muscles

Short description of some CNS diseasesParaplegia

Most common causes 2. Trauma (parasagittal region), 3. Tumor4. TB5. Thrombosis- of sagittal sinus, ACA (uni/ bilat)6. Transeverse myelitis

Quadriplegia Types – spastic & flaccid

Spastic Cerebral palsy, Cerebral anoxia, Brainstem SOL, Syringobulbia, MND, demyelinating disease, Craniovertebral anomaly, Fracture of cervical spine , cervical spondylosis, cervical cord tumors, hematomyelia

Flaccid Poliomyelitis, Polyneuropathy, Guilliane – Barre Syndrome (GBS), Porphyria, diphtheria, Infectious mononucleosis, Polymyositis, Periodic paralysis

Motor neuron diseases Disease (% of total cases) Features Prognosis (years)Amyotrophic Lateral Sclerosis ALS (50 %)

Commonest type UMN & LMN signs (pyramidal tract & antr. Horn)

5

Progressive Muscular atrophy (10%)

LMN signs (antr. Horn) 10

Primary lat. Sclerosis (5%) Onset > 50year, gradually progressiveUMN signs(pyramidal tract)

3

Progressive Bulbar palsy (25%)

LMN signs (cranial nerve nuclei) 2

Pseudo Bulbar Palsy (10%) UMN signs (cortico bulbar fibres) 2Madras MND (More males affected , 10-30 years)

Weakness of facial & bulbar muscles Neural deafnessAbnormal GTT

(Good longevity)

Peripheral neuropathyClassification

1. based on mode of onset Acute <1 week GBS, Porphyria,

Toxins (vincristine), pan- autonomicSub acute 1 week – 1 month - Chronic > 1 month DM, Amyloidosis, Paraneoplastic HIV

Neuropathy, Hereditary Sensory neuropathy

2. based on system affected

Motor GBS, Porphyria, Diptheria, Infectious mononucleosis, Lupus

Toxic- Pb, Al, Thallium, Triortho cresyl phosphate, Opioid Sensory Idiopathic

Toxic – Cisplatinum, Vit B12, Enitro-furantoin, PyridoxineDM, Amyloidosis, Leprosy, HIV

Mixed Drugs- Alcohol, Dapsone, Phenytoin, INH, EMB, amiodarone Metal poison – Au, Hg, PbIndustrial chemicalsHereditary neuropathy, CRF, PBS

3. symmetrical / asymmetrical 4. recurrent – GBS, Porphyria, CPD, Beri-beri

GBS (Guillian Barre Syndrome) Progressive weakness of arms & legs Areflexia, Hypertonia, Plantar flexor Usually Symmetrical Mild sensory symptoms /signs No bladder involvement

Myasthenia Gravis Onset - Insidious / sub acute Ptosis- Uni / bi lateral; Pupils- spared Palatal palsy/ weakness Proximal weakness, weakness more in evening & disappears at rest

Poly myositis Fever, muscle ache & tenderness Symmetrical weakness of proximal & trunk muscles Ocular & facial muscles spared Pharyngeal muscles may be involved Reflexes usually depressed ECG changes Arrhythmia may occur

Myopathies Congenital & familial Onset – gradual & slowly progressive Symmetrically bilat. Selective group of muscles wasted / hypertrophied Kyphoscoliosis No sensory / bladder disturbances

Description of few types of myopathies

Duchenne’s Becker Facioascapulohumeral Limb girdleInheritance Sex linked

recessive Sex linked recessive

Autosomal dominant Autosomal recessive

Onset 3 years 15-20 years 7-25 years 20-30 yearsDistribution of weakness

Proximal > distalPelvic > shoulder

Same as Duchene

Face, arms & scapula Shoulder & pelvic girdle

Cardiac involvement

Common Absent Absent Common

Progress Rapid Slow Slow Variable Prognosis Death 10-30 years Normal Normal Varies