CNS Clinical Notes

CENTRAL NERVOUS SYSTEM HISTORY OF PRESENT ILLNESS 1. Loss of Consciousness / Drowsiness 2. Convulsions 3. Headache 4. Vomiting 5. Deviation of angle of Mouth, Dribbling of Saliva & Inability to Close

Eyes 6. Inabi Inabili lity ty to spea speak  k  7. Difficulty in swallowing, Hoarseness of voice, Nasal Regurgitation,

 Nasal Twang, Dysarthria 8. Smel Smelll – loss 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 –



Triggering factors – Sleep, Exercise, Posture, Reading, Cough, Eating,

progressive / Static / Improving

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) 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 Expectoration 3. Hemoptysis 4. Chest pain & Breathlessness 5. Ear discharge 6.  Fever  – associated exanthema 7. Drug intake- Oral Contraceptives, Phenothiazines, INH, Ethambutol, Vincristine Joint Pain 8. Bleeding Diathesis 9. 10. HT, DM Vaccination, Dog bite (for paraplegia) 11. PAST HISTORY: Head/ Spinal injury 1. Infections – TB, Encephalitis, Sepsis 2. Rheumatic fever (joint pain) 3. h/o STD Exposure, Discharge from Urethra, penile ulcer  4.

5. 6. 7. 8. 9. 10. 11.

h/o Recurrent Abortions/ Still births (STD) Similar Episodes before any Surgery / Drug therapy/ Vaccination Ear discharge  Natal history - full term/ premature, normal/ instrumental  Postnatal history - Jaundice, Infection, Convulsions, Seizures,  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 visual  work under artificial light – tension headache & irritation Overuse of certain joints – carpal tunnel syndrome • •

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PHYSICAL EXAMINATION A. GENERAL EXAMINATION : 1. Consciousness

2. 3.

4. 5.

Comfortable / not Built, nutrition, stature, short neck  Fever   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, subconjunctival Hemorrhage, KF ring, Icterus, Exopthalmos/ Enopthalmos

8.

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

9.

Anemi nemia, a, Pol Poly ycyth cythem emiia, Cy Cyanos anosiis, Cl Clubbi ubbing ng,, 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

B.

14.

Thickened nerves, Trophic ulcers, Joint swelling

15.

Spine – Kyphoscoliosis, Gibbus, Meningocele, Pilodinal sinus

16.

Examination of breast

NEUROLOGICAL EXAMNATION 1. Higher functions a. Consciousness & perception: find if patient is in Coma / Stupor / Delirium; find out any perception disorder  Consciousness disorders state of unconsciousness in which patient does not respond to Coma any type of external stimuli / inner needs  Deep coma = coma + absence of corneal & conjunctival reflexes Semicoma = arousable with preserved reflexes state of disturbed consciousness where patient shows some Stupor  response to vigourous external stimuli like pain conscious but muddled in time, place & person  Disorientatio n state of confusion with excitement & hyperactivity  Delirium patient is awake but lacks impulse to speak / action  Akinetic mutism Acquired global/ multifocal impairment of Cognitive function in  Dementia  presence of normal Consciousness Global paralysis of limbs & cranial musculature, patient is  Locked-in receptive but unresponsive  syndrome

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 Delirium 3. Lesions of Brain stem Reticular activating System

1. 2.

Perception disorders  Delusion – false beliefs [eg: he feels that he has cancer] Common in schizophrenia, GPI, depression  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 hygiene Behaviour – disturbed / apathic/ Agitated / Confused c. Emotional state

Elated, Euphoric, Excited / Depressed Emotional 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 Dysarthria Speech  pronunciation  problem

Dysphonia

Loss of voice

Aphasia

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

Causes i. Bulbar palsy – difficulty in consonants (“p”, “t”, “k”) ii. Cerebellar Disease – “scanning” & Robotic speech. Syllables pronounced individuallly (ask pt. to say “Eyeay”) iii. Pseudo bulbar palsy  – “strangled” & spastic speech, Difficulty with tongue twisters (“British constitution” as “brizh conshishushon”)  Laryngeal disease / innervation defect  Quiet voice => poor ventilatory capacity Fatiguing voice => in Myasthenia gravis, Parkinsonism (slow monotonous speech) (Refer below for causes)

Aphasia: Type

Lesion

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

Sensory aphasia / wernicke’s aphasia

Conduction aphasia

Perisylvian area with damage to fibres of arcuate fasciculus

Transcortical

Motor – antrsuprr to Broca’s area Sensory – postrinfrr to Wernicke’s area Large lesion of middle cerebral artery’s area / l tint. Carotid artery/ trauma

Global

i. ii. iii. iv. v.

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] posterior parieto-temporal region

Characteristics

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

Impaired comprehension of  spoken & written language Fluent speech devoid of  meaning (jargon aphasia) Unawareness of speech deficit Inability to repeat phrases /words spoken by examiner  with normal fluency & comprehension Same as brocas & wernicke’s respectively Marked elements of both  broca’s & wernicke’s aphasia

 Methods of testing  Assess output of speech & fluency Naming of shown objects [eg: pen, comb] Ask to carry out commands like pick up the pencil Repetition of spoken words Writing – find if error inform, grammer, syntax 2. Memory – past & present  Memory  How to test  Remote marriage date, mother or father’s birth date / memory  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 Ask to repeat the numbers / names & in reverse memory 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

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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 •

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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 Ideomotor Ideational apraxia Buccofacial apraxia

Motor disability of onelimb, in absence of gross wkness / ataxia Inability to do the command despite comprehending the command & adqt motor & sensory fntns i.e., defect in execution Loss of ideas behind skiled movements Pt name & describe object but not know how to manipulate it 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 Tactile agnosia

 

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

Visual agnosia

Propasognosia Anosognosia

sensory, motor & coordination normal  Not recog object seen with eyes though visual pathway intact Obj’s color, size are described Inability to identify familiar face Lack of awareness to recog  paralysed limb

Postr. Insula Bilat / left occipitotemporal

Parieto occipital lesion Rt parietal lobe lesion

Handedness – rt / lt g. Sleep duration, intermittent awakening, day time sleeping (narcolepsy), sleep walking & other motor activities (somnambulism), sleep aneuresis f.

Disorders Dyssomnia Intrinsic Extrinsic

Parasomnia Arousal disorders Asso. With REM slp Disorders asso with medical/ psychiatric disorder  Somnambulism Sleep eneuresis

Psychophysiologic, idiopathic, narcolepsy Adjustment sleep disorder, altitude insomnia,food allergy insomnia Confusional arousal, sleep walking  Nightmares, sleep paralysis, sleep related painful erection Mental disorder- schizophrenia, anxiety, depression  Neurological disorder – parkinsomnism, sleep related epilepsy Medical- sleeping sickness, COPD, chronic renal failure, drugs Common in children & adolescents Primary – fsilure to attain continence since birth Secondary – emotional disturbance, UT Infection &malformations, Epilepsy, Cauda equina lesion

Lobar functions & lesions: Personality, emotion, social behaviour   Dominant lobe -language, calculation, appreciation of size, shape, texture & weight  Non-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 Parietal

Frontal lobe Lesions

Unilateral   frontal   Right/ left lobe

Contra lateral spastic Hemiplegia Anosmia [orbital part] Impaired memory

 Prefrontal 

 Bilat frontal 

 Dominant left  lobe

Presence of primitive reflexes [grasping & sucking] Elevation of mood, Talkativeness Loss of initiative Bilateral Hemiplegia, Pseudobulbar palsy Prefrontal lesion-abulia / akinetic mutism, lack of  attention & problem solving ability, labile mood, Primitive reflexes Agraphia, Apraxia of lips & tongue, Loss of Verbal Fluency

Parietal lobe lesions

Cortical sensory loss, mild hemiparesis, homonymous inferior  quadrantanopia, neglect of one half of body In addition to defects in (1) above Disorders of Language[alexia], Gertsman’ syndrome [defect in writing, calculaton, finger agnosia, Right & left disorientation], Tactile Agnosia Bilateral Ideomotor & Ideational Apraxia 3. Non dominant  In addition to (1) Dressing apraxia, Anosognosia, Construction Apraxia, Visuospatial  Rt lobe disorders Visuospatial imperception, topographic memory loss, Anosognosia, 4. Bilat  Construction apraxia, Spatial disorientation

1. Unilat. Lobe  Lt / Rt  2. Dominant Lt  lobe

Temporal lobe lesions

Hallucinations – auditory, visual, olfactory, gustatory Emotional &  behavioural changes, Dreamy state with Uncinate seizures, Homonymous superior Quadrantinopia In addition to (1) 2. dominant Lt. Alexia, Color anomia (Splenium of corpus callosum) lobe 3. non dominant  In addition to (1) Inability to judge spatial relationships in some cases  Rt. Lobe Impairment of non verbal memory Agnosia fo sounds & some qualities of music a. Korsakoff amnesic defect 4. bilateral   b. Apathy & Placidity c. Increased sexual activity d. Sham rage  b + c + d = Kluver Bucy syndrome

1. unilat Rt / Lt 

Occipital lobe lesions Contralat. Homonymous hemianopia – central/ peripheral 1. unilat (Rt /  Elementary Hallucinations in irritativee lesion  Lt) 2. dominant left  In addition to (1)

lobe 3. non dominant rt  lobe 4. bilateral 

Alexia & Color anomia (Splenium of cor. Callosum), Object agnosia in addition to(1) Loss of visual orientation & topographic memory, Contralateral homonymous hemianopia, hallucinations Cortical blindness (pupils reactive) Loss of color perception, Inability to identify familiar faces (Proposognosia)

Cranial nerves

2.

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Olfactory nerve

 Pure motor cranial nerves  Pure sensory cranial nerves  Both motor & sensory cranial  nerves

o o o

3,4,6,11,12 1,2 & 8 5,7,9 & 10

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

Lesions Anosmia: loss of smell sensation Causes - 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 neuritis 2. unilateral loss of vision – Ocular lesions, Carotid hemiplegia 3. defects of visual field (scotoma = characteristic field defects)

Types of scotoma   Name Definition Loss confined to Central Scotoma Central region of 

Types & causes Unilateral  – diseases of Choroid, multiple sclerosis

field of vision Para central scotoma

 Bilateral (biltl) – vit B12 deficiency 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 Concentric constriction

Hemianopia

Concentric constriction of  visual field Loss of vision in one half of visual field

Quadrantanopia

nerve bundle in retina / optic nerve Long standing papilloedema, bilat. lesions of  Striate (visual) Cortex, Retinitis pigmentosa, Hysteria  Homonymous –nasal field of one eye & temporal of other   Heteronymous – loss of nasal / temporal of both eyes  Bitemporal  – lesion of optic chiasm (pituitary tumor), compression in mid-line  Binasal  – lateral compression of chiasma 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)  Efferent lesions (3rd  nerve)

•

III, IV & VI nerves 1. Ocular movements Action of ocular muscle

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

 Elevators  Depressors  Abductors  Adductors  Internal rotators (intorsion )  External rotators (extorsion)

Sup rectus, Inf oblique Inf rectus, Sup oblique Lat rectus, Inf oblique Med rectus, Inf oblique Sup rectus, Sup oblique Inf rectus, Inf oblique

Lesions Diplopia (double vision) Types – Uni & Binocular; Crossed & Uncrossed Due to ocular conditions Uniocular Binocular Weakness of Muscles; Occurs when Eyes are open Paralysis of ADDUCTOR Muscle - Medial, Superior & Inferior recti Crossed  palsy Paralysis of ABDUCTOR Muscle – Lat rectus, Sup & Inf. Oblique Uncrossed  palsy

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

Miotic

5mm

Old age, Horner’s syndrome, Pontine hemorrhage, Drugs like morphine, Neostigmine, Organo  phosphate poisoning 3rd nerve palsy, Optic atrophy, Infants Drugs like Atrophine, Pethidine

Special types of pupil Definition Seen in diseases Argyl Small, irregular, unequal.  Neurosyphilis (tabes dorsalis), DM, Light reflex lost Accommodation encephalitis, Disseminated Sclerosis Robertson pupil reflex preserved, Poor response to mydriatric 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

3. Reaction of light – direct & consensual

4. Accommodation & ciliospinal reflex 5. Nystagmus – vertical / horizontal / rotatory  Definition - Involuntary, Conjugate, Rhythmic oscillations of Eye. Normally occurs on extreme gaze, lasting for 10 secs Types- Pendular & Jerky Definition Pendular Rapid horizontal oscillations to either  side of midline, of Equal amplitude,Seen on forward gaze

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

Types & cause of Jerky Nystagmus : 1. Horizontal To & fro movement of eye ball in horizontal plane 2. Vertical Up & down movement of eye  ball in vertical  plane Osscilatory 3. Rotatory movement of eye  ball whch is rotatory in character 

Rare forms of Nystagmus:

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

Lesions of Vestibular nerve& nuclei, Medial longitudinal bundle, Cerebellum [Nystagmus to the side of lesion] Seen in conditions involving  Brain stem –  Vascular accident, Encephalitis, Multiple sclerosis, Syringobulbia, druds [ anticonvulsants, BZD, Barbiturates], Wernicke’s encephalopathy Seen in Labyrinthine disorders

See saw nystagmus Convergence retraction nystagmus Upbeat nystagmus Downbeat nystagmus Rebound 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

Unilatera l 

involvement) 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 3 rd nerve nuclei •

Trigeminal nerve Motor – temporalis, masseter, Pterygoids Sensory – sensations over the face Corneal & conjunctival reflex Lesions Name Nuclear lesion

Preganglionic nerve lesion

Gasserian ganglion lesions Post ganglionic lesions

•

Affected area Diseases Diseases affecting Tumor, Demylination, Vascular  Pons, Medulla, Upper  lesions, Syringomylia / cervical cord(C2) Syringobulbia Preganglionic Tumors (Meningoma, Assiociated lesions of   Nasopharyngeal carcinoma, other cranial nerves esp Cerebello-pontine angle tumor), VI, VII, VIII Meningeal irritation (Acute / chronic meningitis, Carcinomatus meningitis) (Characterised by Tumors, Abscess, Herpes-zoster  severe facial pain) opthalmicus

-

a. Cavernous sinus lesion  b. Gradenigo’s syndrome c. Superior orbital fissure syndrome

Facial nerve Motor : eye- Frowning, eye closure, Raising of Eye brows, Browing, Mouth & cheek – whistle, showing teeth, nasolabial fold, platysma Sensory: taste in antr 2/3 of tongue Lesions Types – unilat. & bilat.; each being futher divided as upper motor neuron type (UMN) & lower motor neuron type(LMN) Lesions Causes Unilateral  Usually vascular, Cerebral tumor, Multiple Sclerosis UMN  Bell’ s palsy, Parotid tumor, Head injury, Skull base tumors,  LMN  DM, HT  Bilateral  Vascular, Motor neuron disease UMN  Guilian – barre Syndrome (GBS), Sarcoidosis – Uveoparotid  LMN  Fever, Leprosy, Leukemia, Lymphoma

Differences between UMN Bell’s phenomenon (movement of eye ball upwards & inwards on closing eyelids- well seen) Emotional fibres spared Associated with Long Tract signs Exaggerated Jawjerk Corneal reflex present

•

&

LMN type of facial palsy Bell’s phenomenon absent

Emotional fibres involoved Absent Normal Jaw Jerk  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.  Normal ear   Positive Air > Bone   Nerve deafness(sensorineural deafness) Middle ear deafness (conductive  Negativ Bone > Air  Deafness) e Weber’s test: place vibrating tuning fork over middle of fore head,

Point of Application (middle of  forehead) (No lateralization) Better in Normal Ear  (lateralized to normal side) Better heard in Affected Ear  (lateralized to affected side)

 Normal 

 Nerve deafness on Opposite side Conductive deafness on Same side

Lesions of VIII nerve Vertigo = 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 uvula Sensations in posterior 1/3rd of tongue & pharynx

Lesions of IX, X, XI nerves

Bilateral Unilateral

•

•

Palate remains immobile on both sides Dysphagia, Nasal regurgitation, Pharyngeal reflex absent Palatal arch on that side is at lower  level than on healthy side

GBS, Polyneuritis, Myasthenia gravis, Motor neuron Disease 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/ Fasciculations Movement  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 Absent Present Absent Fibrillation Tongue Flaccid Small & spastic Tone Deviation Towards affected side Difficult Protrusion Possible Jaw jerk    Normal Exaggerated

3.

Motor system: a. Nutrition (bulk of muscle) comparing with Opposite side, palpating the muscles i. ii. Note any wasting / hypertrophy & its distribution predominantly Proximal / Distal / Both Feel for muscles Atrophic muscle Flabby Hypertrophic Firm / muscle Rubbery iii. Measure the circumference of limbs

Upper limbs Arm Forearm Lower limbs Thigh Leg

1. 10cm Above Olecranon 2. 10 cm Below Olecranon 1. 18cm Above patella 2. 10cm below Tibial tuberosity

Lesions Hypertrophy – physiological / pathological Muscle wasting 1. generalized 

2. upper limbs i. predominant Proximal muscle

ii. Predominant Distal muscle

iii. small muscle of  hand

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 (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 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

Upper limbs in addition LL

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

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

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

 Diseases Types of rigidity Plastic / lead pipe rigidity

Cog wheel rigidity

gravity Pyramidal lesion (UMN)

gravity Extra pyramidal lesion

Uniform resistance offered to passive1. Parkinsonism (post movement encephalitic) 2. basal ganglia neoplasms 3. catatonia Resistance offered to passive mvmt 1. parkinson’s disease interrupted by alternate contractions 2. over dose of reserpine, of agonist & antagonist muscle due to Chlorpromazine Asso. Tremor  3. carbon monoxide  poisoning

Causes of hypotonia i. lesions of motor side of Reflex arc - Poliomyelitis, Polyneuritis, trauma of peph. nerve ii. lesions of sensory side of “ “ - Tabes dorsalis, herpes zoster, carcinomatous neuropathies iii. combined motor & sensory lesions  – syringomyelia, cord / root compression iv. cerebellar lesions, Chorea Clonus Sudden stretching of muscle produces reflex contraction. If stretch maintained during subsequent contraction further reflex contraction occurs & continues till stimulus removed Dorsiflexion 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 Grade1 Grade 2 Grade3 Grade 4 Grade 5

 No visible contraction Visible musle contraction, but no movement of joints Movement with gravity eliminated Movement against gravity Movement against resistance  Normal power 

d. Coordination upper limb

1. 2. 3. 4. 5. 6.

Outstretched arms test Finger Nose test Nose – Finger Nose test Finger to Finger test Pronation –Supination test Pointing & Past pointing test

4. lower limb

Finger Toe test ii. Heel – Knee test iii. Tandem walking i.

Involuntary movements Name Chorea

Athetosis

Hemiballis mus

Dystonia

Definition Causes & types semi-purposive, irregular,  Lesion in caudate nucleus non- repetitive &brief jerky Genetic  – huntington’s, hereditary movement arising in proximal  Hemichorea – stroke, tumor, trauma, post  joints & appearin g to flit thalamectomy from one part to other   Drug – neuroleptics, phenytoin, alcohol, randomly oral contraceptives Increased on attempting Symptomatic chorea – Encephalitis voluntary movement & lethargica, sub dural hematoma, Exacerbated by emotional Cerebrovascular disease, disturbance hypoparathyroidism, hypernatremia ,  primary polycythemia Slow writhing movement  Lesion in putamen Best seen at wrists (flexing), fingers (writhing), foot (inverted) Proximal joints of one arm Lesion in subthalamic nucleus resulting in Wild, Rapid, Most dramatic of all involuntary Flinging movement of wide movements – may injure patient / radius, occurring constantly  bystanders with short periods of freedom Involuntary sustained muscle Genetic – primary generalized D, Focal contractions frequently adult onset D causing Twisting & repetitive  Heredito degenerative – Ataxia movements telangectasia, Lipid storage diseases, Wilson’s diseases, Parkinson’s disease Symptomatic – Athetoid cerebral palsy, cerebral anoxia, post-encephalitic dystonia  Drugs – neuroleptics, Mn poisoning,

Tremors

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

Myoclonus

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

Tics

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

Fasciculatn

Irregular, non rhythmic contraction of muscle fascicles Contraction of individual muscles

Fibrillation

Titubation

f.

Involuntary nodding of head

Levodopa  Hemidystonia – stroke, trauma, tumor, AV malformations Rest tremors – parkinson’s disease, post encephalitic parkinsonism, drug induced  parkinsonism Postural - physiological, thyrotoxicosis, anxiety, alcohol, caffeine Intentional – lesions of cerebellum & its connections in diseases like multiple sclerosis, Spinocerebellar degeneration, tumor  Generalized – progressive myoclonic encephalopathies, hereditary myoclonus, metabolic (Tay- sach’s & Batten’s disease), Alzheimer’s disease Metabolic – Uremia, hyponatremia, hypocalcemia, hepatic failure Drug induced, alcohol & drug withdsnal Focal / segmental – spinal tumor/ infarct/ trauma, palatal myoclonus Simple tics – transient tic of childhood, chronic simple tic Complex multiple tics – chronic multiple tics Symptomatic tic – encephalitis lethargica, drug induced, post traumatic Motor neuron disease, syringomyelia, cervical spondylosis, peroneal muscular  atrophy, poliomyelitis (in recovery stage) Denervation hypersensitivity Easily perceived over the tongue where they are easily seen under mucus membrane Lesions of Vermis of cerebellum

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

Seen in Hemiparesis

Spastic gait

Lesion of UMN involving  both lower limbs Marked spastic gait as in cerebral diplegia

Scissors gait

Description Pt. throws his lower limb outwards at hip joint (circumduction), & leans towards opposite healthy side Affected arm adducted at shoulder & flexed at elbow, wrist & fingers Adductor spasm causes legs to cross each other & each foot trips the other  Marked spasm of adductors of lower  limbs

High stepping gait

High stepping & stamping gait

Ataxic gait

Shuffling gait

Waddling gait

Pts with foot drop

Pt raises foot high to overcome foot drop & on keeping foot down toe hits ground first There is no ataxia Posterior column lesion Pt not know where his foot is & so on (gross loss of position walking raises foot high up in air & sense)  brings it down forcefully (stamping gait), heel touches ground first More prominent in dark / pts ‘ eyes closed Cerebellar lesion Pt is ataxic & reels in any direction including backwards & walks on a  broad base Difficulty in tandem walking Extra pyramidal lesion Series of small flat footed shuffles Associated with rigidity Parkinsonism – pt. stooped posture esp. Parkinsonism (universal flexion) & walks in small, shuffling steps as if trying to catch up with center of gravity Automatic assoc. upper limb absent Primary muscular disease- Pt walks with broad base with  proximal weakness of  exaggerated lumbar lordosis lower limbs(muscular  dystrophy)/ bilateral hip  problem (congenital dislocation of hips)

 Lesions of Extra pyramidal system Sign Resting tremor Muscular rigidity Hypokinesia Chorea Hemiballismus Dystonia, Athetosis

Site of lesion Substantia Nigra, Red nucleus SN, Putamen SN, Putamen, Globus pallidus Caudate nucleus Sub – thalamic nucleus Putamen

Signs & symptoms of Parkinson’s disease & Parkinson plus syndrome (progressive  supranuclear palsy, Dementia with Lewy bodies, Multiple system atrophy) Feature Tremor  Tone

Movements Thought   process

Parkinson’s disease Rest tremor (pill rolling) Rigidity -cogwheel (best seen in UL) / lead pipe(best seen in LL & trunk) Bradykinesia Bradyphrenia (slow thought)

Parkinson plus syndrome Action tremor & impotence Marked axial rigidity

-

Saccades &  pursuit  movements  Facial  expressions  Handwriting   Posture Gait   ANS  dysfunction

Slight jerky saccades Pursuit eye movements Facial hypomimia (lack of facial expression) Micrographia (small hand writing) Stooped Festinant (short shuffling gait) Mild

Vertical supranuclear  saccade (PSP) Broken pursuit (MSA) Falls early in disease course Ataxic 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 Lower cervical T1-6 T7 -9 T10 T11 T12 L1

ii.

Segmental level of spinal cord +1 +2 +3 Overlies L1 & 2 “ L3 & 4 “ L5 “ sacral & coccygeal segments

Posterior column sensations 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  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  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 sensations 1. Tactile localization Ability to correctly localize pt. touched with head of pin / finger  tip 2. Tactile discrimination Finger pulp & lips 3-5 mm well recog. Palm 2-3 cm Sole 4 cm Dorsum of foot, > 5 cm Legs, Back  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 Contralat loss of only  Exteroceptive sensatn Contralat loss of only  Proprioceptive sense Contralat loss of Position sense

extensive lesion of thalamus, usually vascular  Partial lesion of thalamus, Lesion in lat. Part of brain stem  partial lesion of thalamus, lesion in medial part of brain stem  parietal lobe lesion / lesion between thalamus & cortex

& Cortical sensatn + disturbance of light touch &  pain contralat Hyperalgesia &

 partial lesion of thalamus

 Hyperesthesia  Loss of Pain & Temp on Same

Lesion of medulla affecting descending root of V nerve &

 side of Face & Opp. Side of 

asc. Spinothalamic tract of rest from rest of the body

body Unilat. Loss of pain & temp

Brown Sequard syndrome

below definite level  Glove & Stocking anaesthesia,

lesion of peripheral nerve / sensory root as in diabetes

(all sensation lost over a clearly

mellitus, polyneuropathy, mononeuritis multiplex

defined part of body like area of  glove & stoking)  Patchy area of sensory loss

chronic polyneuritis, Leprosy, tabes dorsali mononeuritis

loss of sensation of Saddle type

multiplex 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

loss of Vibration sense alone

retained if affecting lower limbs =>intrinsic cord lesions like

loss of Position & Vibration

multiple sclerosis, syringomyelia  postr. Column lesion as in tabes dorsalis,

only

subacute combined degeneration

Reflxes: Superficial reflexes 5.

i.

 Reflex  Corneal 

Conjunctiva l   Pharyngeal 

Technique Corneal edge with cotton wisp, Pt look in opp. Direction Bulbar conj. With wisp of  cotton Posterior pharyngeal wall tickled

 Palatal 

Soft palate tickled

Scapular 

Stroke skin in interscapular area

 Abdominal 

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

Cremasteric

Upper & inner part of  thigh stroked downward & inward direction

 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 metatarsophalangeal  joints

Segm. Innervation Afferent – V nerve Center – pons Efferent – VII nerve -do-

Normal result Brisk closure of eyes

Aff – IX nerve Cen – medulla Eff – X nerve Aff –V nerve Cen – medulla Eff – X Aff – C4-5 Cen – C4-5 Eff – dorsal scapular  nerve Upper abd: T7- T9 Mid :T9- 10 Lower: T11,12

Contraction of   pharyngeal muscles

Aff – femoral nerve Seg – L1,2 Eff – genitofemoral nerve Aff – tibial nerve Seg – L5, S1,2 Eff – tibial nerve

Clinical Significance of Babinski’s sign 1. Lesions of corticospinal tract (pyramidal tract) 2. infancy ( upto 1year)

-do-

Soft palate moves up

Contraction of scapular  muscles

Muscles in quadrant stimulated contract & umbilicus moves in that direction Contraction of  cremasteric muscle  puls up scrotum & testicle on that side Big toe flex at metatarsophalangeal jt. & flexion of other toes Babinski’s sign –  extension of big toe with extension & faning out of other toes

3. 4. 5. 6. 7.

deep sleep deep anesthesia narcotic overdose alcohol intoxication 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 side 2. Gordon reflex – calf muscles squeezed 3. Chaddock reflex – light stroke below lat. malleolous

ii.

deep reflexes Spinal segment involved Biceps C5 Triceps C7 Supinator C5, 6 Hoffman C7, 8, T1 Knee L3, 4 Ankles L5, S1 Pectoral C7 Deltoid C5 All reflexes should be tested on both sides 0 1 2 3 4

Absent Present as Normal jerk  Brisk as a normal Knee jerk  Very brisk  Clonus

Grading

iii.

Inverted reflexes Reflex  Inverted  radial  reflex

 Inverted  biceps  Inverted   Knee reflex

Procedure Supinator jerk => absence of elbow flexion but there is finger flexion Biceps jerk absent & triceps exaggerated Biceps reflex => no flexion of elbow  but extension of elbow due to triceps contraction Knee jerk => no extension instead flexion of knee due to contraction of  hamstrings

Lesion Presence => C5,6 segment lesion

Presence=>C5,6 segment lesion Presence=>Lesion of L2,3,4

Other allied reflexes Procedure Reflex  Hoffmann reflex

Wartenberg’s reflex

v.

vi.

Lesion

Terminal phalanx of pt’s mid finger  In hypertonia tips of other  flicked downwards between fingers flex & thumb flexes examiner’s finger & thumb and adducts Pt’shand supinated, slightly flexing  Normally thumb extends but fingers with thumb in adduction , terminal phalanx may flex Examiner pronates his hand & links slightly his hand with that of pt’s fingers. In hypertonia => thumb Both flex their fingers & pull adducts & flexes strongly against each other’s resistance Indicating pyramidal tract lesion

sphincteric reflexes ask the pt. for difficulties in Swallowing, Defecation, Miicturition, Sexual function  primitive reflexes (released reflexes) Deficit of  frontal  function release primitive motor behavior which includes following reflexes Reflex  Pout  reflex

Description Rubbing of chin causes pouting / “sucking” lip movements

Grasp

Pt tends to grasp objects esp

reflex

examiner’s fingers when they are

Clinical inference Polysynaptic reflex released by frontal lobe disease / diffuse degenerative brain disease -

 placed in his palm, esp in contact  between thumb & index finger   Palmo Scratching the palm produces mental  unilateral contraction of mentalis muscle reflex

 Non specific sign sometimes seen in normal people also

6. Autonomic nervous system i. check pupillary response to light & accommodation ii. skin –dryness => absence of sweating iii. resting tachycardia- present / not iv. pulse rate slowing with deep inspiration v. trophic changes in distal skin – absence of hair growth, nail  bed  Bladder Innervation Innervation

Segment

Part innervated

 Parasymp.  Emptying  Symp. (also carries pain  sensation ) – filling  Somatic

Types of Bladder &  Incomplete spastic /  uninhibited bladder 

Complete spastic / reflex /  automatic / hypertonic bladder   Autonomous bladder /  hypotonic Sensory paralytic (afferent   pathway lesion )

 Atonic bladder (reflec arc lesion) Motor paralytic (efferent   pathway lesion )

S2,3,4 T11, 12, L1,2 S2,3,4

Detrussor muscle via pelvic nerve Trigone muscle via presacral & hypogastric nerves External sphincter & perineal muscle pudendal nerve

Levels of Lesions, clinical condition  Post central  – loss of awareness of bladder fullness, incontinence  Precentra l – difficulty in initiating micturition  Frontal – inappropriate micturition, loss of social control (like infant’s bladder) Lesion in spinal segments above S2,3,4

Lesion at S2,3,4 & Cauda equina Seen in DM, Syringomyelia, Tabes dorsalis Intact voluntary initiation of micturition Urinary retention- overflow incontinence Frequent urinary tract infection Seen in Tabes dorsalis, Conus & Cauda Seen in lumbar canal stenosis Lumbo-sacral meningio- myelocele Painful urinary retention

7. Cerebellar signs Part  Archicerebellum  Paleocerebellu m  Neocerebellum

Connected to Vestibular nuclei Spinal cord

Function Maintain equilibrium Maintain posture

Cerebral cortex

Center of voluntary movements

Parts

Lesions of cerebellum Clinical signs 1. Hypotonia , 2. Dysmetria (inappropriate range of movement) 3. Intention tremor  4. Adiadochokinesia 5. Rebound phenomenon

6. Nystagmus – quick & towards direction of gaze, occasionally skew deviation in acute lesions 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 Causes

1. 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. Alcohol 6. 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 Loss of cervical laordosis Increased lumbar  lordosis Loss of lumbar  lordosis iii.

Ankylosing spondylitis Acute lesions, rheumatoid arthritis, cervical spondylosis Muscular dystrophies Acute disc collapse, aging, ankylosing spondylitis

Scoliosis = lateral curvature of spine Postural, congenital, unequal limb in length, acute disc collapse, Extensive fibrosis of lungs, inflammatory disorders

v.

 Kyphoscoliosis = lateral + posterior bending of spine (kypho = backward bending) Congenital, poliomyelitis, neuromuscular disorders Tenderness

vi. vii.

Height- neck ratio Auscultation over skull

iv.

b. Signs of meningeal irritation Usually meningitis, sub-arachnoid hemorrhage

Sign i.  Neck   stiffness

Procedure Passively but gently flex pt’s neck 

Normal chin touch chest without pain

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

ii.  Kernig’s  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. iv.

Brudzinki’s sign 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 CNS Blood supply of cerebrum Artery  Anterior  cerebral  artery

Middle cerebral  artery

Area supplied Entire Mdl surface + 2 cm strip along Superolat surface & Mdl ½ of Orbital surface Entire Ltl surface + Lat ½ of orbital surface Superior divisison  broca’s area Inferior division Wernick’s area

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

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

 Posterior  cerebral  artery

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

Terminal occlusion=>visual cortex 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. medulary f. postereior inferior cerbellar   Infarction of posterior inferior cerebellar artery Infarct Level  Paramedian infarct 

 Basillary infarct   Posterolat  infarct  (wallenberg’ s  syndrome)

Regions involved 12th nerve nucl, mdl lemniscus & medullary  pyramid infr olive & pyramid

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

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

Contralat ataxia & motor adaptation failure and contralat hemiplegia Ipsilat horner’s, facial numbness & ataxia, loss of contralat pinprick  sensation & vestibular disturbance, speech & swallowing difficulty

Basilar artery branches

1. Pontine artery 2. Labyrinthine artery 3. anterior inferior Cerebellar artery  Infarction of anterior inferior cerebellar artery Infarct Level

Regions involved

Clinical Effects

 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  Paramedian infarct 

Regions involved Red nucleus & 3 rd nerve nucleus

Clinical Effects 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 artery

Stroke •

• • • •

• •

• •

•

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

2. evolving stroke

Rapid onset Persistent ND that does not progress beyond 96 hours Gradual step wise development of ND

3. transaient ischemic attack  4. Reversible Ischemic  Neurological Deficit (RIND)

Focal ND resolves completely within 24 hours 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  Lower cervical  T1-6  T7 -9 T10 T11 T12  L1

•

Position of fibres Column  Posterior  column

 Lateral &  Anterior Column •

Segmental level of spinal cord +1 +2 +3 Overlies L1 & 2 “ L3 & 4 “ L5 “ sacral & coccygeal segments

Position of Fibres Fibres from Lower Limb are placed medially near  central canal & from Upper Limb are placed laterally Corticospinal & Spinothalamic tracts

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

Touch , Position, movement, Vibration & pressure sense Cervical, thoracic, lumbar, sacral

•

Lesions o

 Localization of segmental level  Order 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  Foramen magnum

signs Atrophy of sterno mastoid muscle

Downbeat Nystagmus C2 sensory loss & cerebellar signs Horner’s syndrome

Cervicomedullary

Lower cranial nerve palsy Paralysis of ipsilateral lower limb & contralateral UL

 junction

(due to arm fibress ccrossing before the leg fibres at

(hemiplegia

lower part of medulla)

cruciata) C2 segment 

C3

1. Sub-occipital pain / sensory loss 2. Descending tract of Vnerve (pain & temp. loss over face 3. Exaggerated trapezius reflex Loss of trapezius reflex

C5

1. Inverted biceps jerk  2. Inverted brachioradialis jerk (supinator jerk) 3. Sensory loss over deltoid

C6 

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

C7 

1. 2. 3. 4.

C8 & T1

1. Weakness & wasting of small muscles of hand 2. UMN signs in lower limb 3. Uni / bilat. Horner’s syndrome

Paresis of flexors & extensors of wrist & fingers Preservation of biceps & supinator reflex Exaggerated finger flexor reflex Inverted triceps reflex

T3

1. Girdle pain / paraesthesia 2. Segmental LMN involvement 3. ANS dysfunction Sensory impairment in axilla

T4

Sensory impairment below level of nipple

T6 

Abdominal reflex impaired

Thoracic segments

T10

+ ve beevor’s sign (intact upper abd reflex & absent lower  abd. Reflex with pull of umbilicus >3 cm on raising the head) 1. Abdominal reflex preserved

T12

2. 3. 4. 1. 2.

 L3, L4

3. 1.

S!, S2

2. 3. 4.

Sensory loss in LL staring from level of groin Brisk ankle & knee jerk  Absence of cremasteric reflex Hip flexion preserved Atrophic paralysis of quadriceps & adductors of  hip Loss of knee jerk & ankle jerk  Atrophic paralysis of intrinsic muscles of foot, calf muscles Knee jerk preserved Ankle jerk & plantar reflex lost Anal & bulbocavernous preserved

1. Saddle anesthesia 2. Bladder & bowel involved 3. Normal reflexes in LL

S3, S4

Compression of spinal cord

 Effects of compression Slow spinal compression affects First the pyramidal tract  Next posterior column Spinothalamic tract LMN signs

 Anterior horn cell   Posterior root   Posterior column  Pyramidal tract 

LMN signs (weakness, wasting, fasciculation) Root pain/ girdle pain (trunk) Lhermitte’s sign (unpleasant / electric sensation) Constriction band around trunk  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

Less common

1or 2 segments at site of root compression  Not common Rare

Wide due to antr. Horn involvement Present Common

Sensory Root pain ………………. Common Funicular ………………..  Not present Dys& paraesthesias……… Rare Dissociated sensory loss…. Absent Sacral sensation…………. Lost

Joint position sense ………. Lhermitte’s sign …………. ANS Bowel & bladder disturbance  Investigation X-ray of spine …………… Effect of lumbar puncture ….

Lost Present

Rare Present Common Present Sacral sparing for Pain & Temp Spared Absent

Late

Early

Bony changes seen Signs & symptoms are  pptd / increased

 Not seen  No such effect

2. Mode of onset Vertebral pain (local tenderness)

Extra-dural & Intra dural lesion Asymmetrical Symmetrical Uncommon Common

3.

Lesions of Conus medullaris Symmetrical Onset Disso. Sensory loss Present Root pain Rare Rare Fasciculation Decubitus ulcer Rare Early Bladder & bowel

4.

Lesions of Bladder involvement Faecal incontinence Saddle anesthesia Motor symptoms

Conus medullaris Distension

Cauda equina Asymmetrical Absent Common Common Common Early / late depending on root involvement

&

Epiconus

-

Present

Absent

Present Absent

Absent Paralysis of LL

muscles

Short description of some CNS diseases Paraplegia Most common causes 2. 3. 4. 5. 6.

Trauma (parasagittal region), Tumor   TB Thrombosis- of sagittal sinus, ACA (uni/ bilat) Transeverse myelitis

Quadriplegia Types – spastic & flaccid

Spastic

Flaccid

Cerebral palsy, Cerebral anoxia, Brainstem SOL, Syringobulbia, MND, demyelinating disease, Craniovertebral anomaly, Fracture of cervical spine , cervical spondylosis, cervical cord tumors, hematomyelia Poliomyelitis, Polyneuropathy, Guilliane – Barre Syndrome (GBS), Porphyria, diphtheria, Infectious mononucleosis, Polymyositis, Periodic  paralysis

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

Progressive Muscular  atrophy (10%) Primary lat. Sclerosis (5%) Progressive Bulbar palsy (25%) Pseudo Bulbar Palsy (10%)

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

Prognosis (years) 5

Onset > 50year, gradually progressive UMN signs(pyramidal tract) LMN signs (cranial nerve nuclei)

3

UMN signs (cortico bulbar fibres)

2

Madras MND Weakness of facial & bulbar muscles (More males affected , 10-30  Neural deafness years) Abnormal GTT Peripheral neuropathy Classification 1. based on mode of onset 1 month

10

2

(Good longevity)

GBS, Porphyria, Toxins (vincristine), pan- autonomic DM, Amyloidosis, Paraneoplastic HIV  Neuropathy, Hereditary Sensory neuropathy

2. based on system affected

Motor 

GBS, Porphyria, Diptheria, Infectious mononucleosis, Lupus

Sensory

Mixed 

Toxic- Pb, Al, Thallium, Triortho cresyl phosphate, Opioid Idiopathic Toxic – Cisplatinum, Vit B12, Enitro-furantoin, Pyridoxine DM, Amyloidosis, Leprosy, HIV Drugs- Alcohol, Dapsone, Phenytoin, INH, EMB, amiodarone Metal poison – Au, Hg, Pb Industrial chemicals Hereditary 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       

Inheritance Onset Distribution

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

Sex linked recessive 3 years Proximal > distal

Sex linked recessive 15-20 years Same as

Facioascapulohumera l Autosomal dominant

7-25 years Face, arms & scapula

Limb girdle

Autosomal recessive 20-30 years Shoulder &