Includes Muscle Power Testing video a - Z SV Khadilkar GS Soni Second Edition CBS www.nationalbookdepot.com CBS Publishers & Distributors Pvt tis Scanned with CamScannerNeurology Simplified By SV Khadilkar MD DM DNBE (Neurology) Hon. Professor and Head, Department of Neurology Grant Medical College and Sir J J Group of Hospitals, Mi Consultant Neurologist, Bombay Hospitals, Mumbz Ex President, Maharashtra Association of Neurolor President elect, Bombay Neurological Associatio Editor in chief, Annals of Indian Academy of Neurc GS Soni MD DM (Neurology) Associate Professor (Consultant) Department of Neurology Grant Medical College and Sir J J Group of Hospital SECOND EDITION www.nationalbookdepot.com 7 CBs CBS Publishers & Distributors Pvt ita Scanned with CamScannerpach “HM Approach @ Approach t 4, Approach Approach G) Approach Approach Approach Approach 7, a a -@ ©. 2, Headache 3: & 8, CONTENTS to Hemiparesis » Paraparesis (t o Cerebellar Ataxia #4 to Hypokinetic Movement Disorders £0/nAlasti Pof-t1R(0 46 to Hyperkinetic Movement Disorders : 5 to Gait and Its Disorders .,l/A.i. $0 2 SRT 73 to 79 to Patient with Myopathy 2¢ 6 LLG Ge 96 8p to Cranial Neuropathies :t Mula. pala Bex tus Examin 5 Approach to Patient with Coes Impairment/Mental S Epilepsy fedadeiy ete nce . so Multiple Sclerosis and other Demyelinating Diseases... 7 Neuromuscular Junction and its Disorders 491 Approach to Dizziness/Vertigo .. st 16, Neuroradiology ... iene 17. Appendix Index... A, (Proformas).. Scanned with CamScannerAPPROACH TO HEMIPARESIS Hemiparesis is weakness on one side of the body. It is less severe than hemiplegia; the total paralysis of the arm, leg and trunk on one side of the body. Meticulous motor system examination is very important in patients with hemiparesis) or quadriparesis. Hence we shall initially discuss details of motor system examination. MOTOR SYSTEM EXAMINATION The following points are noted while performing motor system examination. ead Nutrition /Qut< Power * ‘Tone Reflexes ee eiments Gait Se ae Upper motor neuron (UMN) lesions are characterized by weakness, spasticity, hyperreflexia, Babinski sign and absent superficial reflexes, primitive reflexes may appear. Primitive reflexes include the grasp, suck and snout reflexes, Lower motor neuron (LMN) lesions are characterized by weakness, hypotonia, hyporeflexia, atrophy and fasciculations. ran Wane 1. NUTRITION Muscle bulk can be evaluated by comparing the size and contours of muscles bilaterally. Atrophy is evidenced by flat or concave muscles, Muscle wasting is common in LMN lesions, Wasting can occur commonly in chronic hemiplegia; due to disuse atrophy, Detection of wasting ean be done by doing measurement of muscle girth/bulk of limbs from fixed bony points, In one method, following are fixed points used for muscle bulk measurement in grown up adults, Distance can vary from case to case, . Motor neuron disease _Myotonia congenita Arm : 10 cm above the olecranon Forearm : 10 cm below the olecranon ‘Thigh ; 18 cm above the upper border of patella Leg : 10 cm below the tibial tuberosity Following are common causes of mus hypertrophy. pore aychenwie dis ac 7 Ne Muscle atrophy/wasting: flabby iniisctes Poliomyelitis Spinal muscular atrophy Intramedullary cervical cord lesions (Upper limb atrophy) Hereditary sensory-motor neuropathy Advanced myopathy or muscular dystrophy =" Multifocal motor neuropathy Comal Comite, anal gue emyeboa Musa yertrophy: Rubbery or firni feel” {itichenne and Becker muscular dystrophy Limb Girdle muscular dystrophy Hypothyroid myopathy Infiltration of muscles (amyloidosis, neuro- cysticercosis) Chronic S, radiculopathy (calf muscles only) joeaslepesttee Muscle strength is graded from 0-5 (Medical research council grading), 0 = no contraction 1 = barely detectable flicker or trace of contraction; but no movement of joint active movement with gravity eliminated (Horizontal movement is possible) active movement against gravity active movement against gravity and some resistance, active movement against full resistance (Normal), Scanned with CamScannerHxaminer compares patient's right side to left side, “5, to detect asymmetry; patient's dominant side may be slightly stronger Neurology Simplified Hamstrings - L,, 8,, 8,; sciatic 6. Knee extension : Quadriceps - Ly L,; femoral Examiner tests the muscle strength of upper extremities (arm, forearm and hand), lower extremities (thigh, leg and foot), neck and trunk 7: Ankle dorsiflexion : Tibialis anterior « Ly 1 muscles. fe csbriohts - Cu pwsiaploh Mave ‘up peroneal nerve. etree Boe Scopalos ries 8, Ankle plantar flexion : Gastro-soleus - S,, Upper extremities © [°**)~ eto ctovet Sew tibial nerve. 1. Shoulder-abdi Supraspinatus (first 1g°) 9. Ankle inversion : Tibialis posterior ~ L,; tibial C. Supra nerve and Deltoid - C,, nerve. tp TA in teen axillary nerve. Lay hi 5 Seu 10. Ankle eversion’: Peroneus longus and brevis 2 Shoulder adduction Poctoralis pai and minor «Ly. 8,: peroneal nerve. ‘ loop p anG toral nerves: eee Oe te 2 ch ne 3 . Set fee 11. Great toe exten fensor hollucis longus 3. Shouldér flexion and extension : Deltoid <3; pororea) waine anterior and posterior fibers respectively - C. cillary nerve {ISS lei ret 2Ee4_ 12. Great toe flexion : Flexor hollucis longus ~ 15 trier ~WeliaCeer) + hatiiaees , Tibial nerve 4. Elbow flexion Biceps - C,, C,, musculo- GA Pplyg - Adde tet cutaneous nerve. Axial muscles: ~_ _ 5. Elbow extension : Triceps - C,; radial nerve, 1, Neck flexion : B/L sternocleidomastoid; Spinal 6. Wrist flexion : Flexor digitorums, Flexor carpi ecameeatineie ulnaris and Flexor carpi radialis 2. Neck extension : Nuchal muscles - C,, C, and ulnar nerves: Occipital nerve 7. Wrist extension : Extensor indices, Extensor 3, Trunk flexion : Paraspinal muscles - Thoracic carpi ulnaris and Extensor carpi radialis-C,,C, nerve rootlets. saath neces 4. Abdominal muscles (1,T,,) 8. Hand grip : Finger flexors - C,, C,, T,; median and ulnar nerves. 9. ‘Thumb opposition : Opponens pollicis - C,, T,: median nerve. POWER TESTING OF IMPORTANT MUSCLES 1. Deltoid : (C,) “Ayillory ewe » Pationt is asked io hold the arm abducted to 60° (S aa eae ere va i C- ieesiret cratiinerokestaae ane zi ast 98 waters soe inatus :(C,) Serascapoloes ver Palmar intorosse: Cs ‘The patient tries to initiate abduction of the arm (\ none from side against examiner's resistance, s) 2 Abduction of fingers : Dorsal nterossel: Cg, homboids:C,) Da cca a Hands on hips and patient asked to force his | Lower extremities (0. 1, elbow backwards against resistance. ) et haba peel tn ior : (C,, C,,C, = Nerve of Bell) | _ 1. Hip flexion :Miopsoas -1,, L3L;;fémoral nerve. * Serratus anterior : (C,, Cy C, exten: i |= ‘The patient asked to push the arm against 2. ¥ 2 2 ae pease ve 3) the wall with straight elbow, : for Sai ierantion Lower limb : Babinski's trunk-thi Patient is asked to get up from supine position without support. If there is © Intrafusal muscle fibers; innervated by gamma Hocclev ee tes tna: tet ees oa fusal fibers and are responsible for'tone. They be elevated Irom the bed (leg raising are controlled by supraspinal innervations a (pyramidal as well as extrapyramidal systems), ». igiiy + Tone is usually more in antigravity group of eer dependent (same resistan ‘iitéala ependent (same resistance: ven with increased speed of movement) = In upper limbs ~ tone is more in flexors than a “! oe nore in flexors than Seen in exteapyramidal lesions (Parkinson's isease), = Inthe lower limbs ~extensor predominance ‘Agonist and antagonist musctos are equally Method of testing a » Dims Lead pipe or cogwheel phenomenon is ‘The patient is asked to relax. ‘The examiner supporls the patient's elbow and grasping the Best way to detect \y patient's hand, passively flexes and extends the + At wrist joint: Slowly wrist is rotated | wrist, shoulder the moderate smoothly; resistance offered to passive range of motion. Normal resistance is fell as mild movement is interrupted by alternate | resistanceeto passive st evenly throughout £0 and antagonist | the entire range of the Lal each joint muscles due to associated tremors (C08 + Lower limbs wheel rigidity) ‘The patient is asked to relax. ‘The examiner > Fromit’s mane Patient is asked 10 supports the patient's thigh behind the kne Hernating closure and opening grasps the patient's foot with the other ly movement of the hand not being tested oF passively flexing and extending the knee and asked to concentrate on the fan/light: while 1 ankle in a single and smooth mavament Wocking lor rigidity. This mance bnings out cogawheel rigidity in the tested hand ; = i pe i Scanned with CamScannerNeurology Simplified Causes of winging of scapula Due to serratus anterior muscle weakness (whole medial border of scapula elevated). ‘ ; bocads Sometimes it is caused by trapezius/Weal doch (only inferior angle of scapula elevated) Seen in radiculopathy (brachial plexus injury) Fascioscapulo-humeral muscular dystrophy. Limb girdle muscular dystrophy. ig. 1. Winging of scapula (seen in resting position. Clinically evident when patient is asked to bring outstretched upper 5s downwards) Infraspinatus : (Cx)! :) ees fee Patient is asked to stand with elbow’flexed at his side and instructed to rotate arm externally (laterally) against resistance. 6. Teres major (C-C,) Lover ceukscoptar reve Patient is asked to stand with elbow flexed at the side and instructed to rotate arm interfi (medially) against resistance, Sternal head : Hand is placed on the hip and trying to push arm inwards against resistance. Clavicular head : Arm is raised forward to 90° and trying to adduct it against resistance. ‘Test grade 3 power in pectoralis : In supine/ Icke) position; patient is asked to adduct both uppet limbs. 8. Latissimus dorsi: (C,) Tho* Abdominal reflex - Cremaster reflex: + Plantar response ‘The "anal wink" is a contraction of the external anal sphincter when the skin near the anal opening is scratched. This is often abolished in spinal cord damage (along with other superficial reflexes). Cremastric reflex (L,) + In supine or standing position, stroke is given over inner upper aspect of thigh from above downwards and inwards + Normal respon is upward movement of testes due to contraction of cremaster mus’ contraction, Absent in + Pyramidal tract lesion > LMN lesion at L, + Non-neurological condition where cremastric roflex is lost/diminished : Abdominal reflex (1,21) ‘Tested by stroking of the abdomen around the umbilicus, Scanned with CamScannerposition, uncover the abdomen and see that abdominal muscles are well relaxed. With a blunt object gently stroke on the abdominal skin from lateral to the medial aspect in all the four quadrant © Observe the contraction of the abdominal muscles resulling in deviation of umbilicus towards the area stimulated. © Anormal positive contraction of the abdom umbilicus moving towards the stimulation. Abdominal reflex and Gremastric reflex Lost in UMN lesion. Lost in UMN lesion sponse usually involves a nal muscles and the source of the dysfunction. In congenial diplegia/cerebral palsy and motor neuron disease - nol lost till Tate. Lost very early in'multiple sclerosis” Plantar response : (Tibial nerve; L,-S,) Method: * Place the patient in a supine position and tell that you are going to scratch the foot, first gently and then more vigorously. + Fixate the foot by grasping the ankle or medial surface with the examiner's hand. + Begin with light stroking, using fingertip or nail; then use a blunt object such as the point of a key. + The first line to be stroked begins a few centimeters distal to the heel and is situated at the junction of the dorsal and plantar surfaces of the foot (lateral asp line extends to a point just behind the toes and then tums medially across the transverse arch of the foot. Stroke slowly, taking 5 or 6 seconds to complete the motion, (in early pyramidal dysfunction, lateral plantar stimulation is more likely to elicit Babins response. Usually stimulation of medial plantar area elicit grasp reflex; but can also Babinski’s response in severe pyramidal dysfunction). + Normal response is flexion of toes (toes all curve inwards). This response is seen in healthy adults with a fully developed and functional central nervous system, © NoResponse: Indicates damage to the peripheral nervous system, muscles, or thick skin. Babinski Response/sign Refers to an extension of great toes with or without fanning of other toes and withdrawal of leg due to pyramidal dysfunction. @) ) Fig. 2. (a) Normal plantar response (b) Extensor plantar response Pathways ‘Afferent: Nociception detected in the S, dermatome and travels up the tibial nerve to the sciatic nerve to roots of L,, S, and Synapse in th je anterior horn to elicit the motor respons Efferent: Motor response back through the L,, 8, roots to the sciatic nerve to its bifurcation. Toe flexors are innervated by tibial nerve. Toe extensors (extensor hallicus longus, extensor digitorum Jongus) are innervated by the deep peroneal nerve. Loss of normal adult de: dal control The reflex arc to suppress extensor withdrawal results in the upgoing toes in the plantar reflex own as Babinski's sign. Muscles taking part components of Babinski Extensor hallucis longus (EHL) (Great toe extension) _ Extensor digitorum longus (Fanning of toes) Tibialis anterior (Dorsiflexion of ankle joint) = Hamstring group of muscles (Flexion of knee joint) lata (Flexion of hip joint) in Babinski's sign and sign are = Tensor fase Rules of interpretation of the Babinski sign «Groat tov extension is pathological only if caused, by contraction of extensor hallucis longus muscle. «© Contraction of extensor hallucis longus muscle is pathological only if it occurs synchronously with reflex activity in other flexor muscles «A true up-going toe sign is reproducible, unlike withdrawal refle: Scanned with CamScannera = Causes of Babinski sign Pyramidal tract dysfunction Up to the age of 1.5-2 years Deep sleep Comatose patients Following seizures Hypoglycemia Narcosis Following electroconvulsive therapy ‘+ Abnormal reflex seen as extension of the big to .ABing sign - multiple pinpricks on the dorsum of the foot, Cornell sign - scratching along the inner side of Chaddock sign - stroking the lateral malleolus, ~ Gonda sign - flexing and suddenly releasing the 4th toe, = squeezing the calf muscle, Gordon Schaeffer sign - squeezing the Achilles tendon. 1 Bled epion anddenbd + Abnormal reflex seen as flexion of toes Mendel reflex - flexion of the 2nd to Sth toes on Rossolimo sigal “Eaperale Babinski-lil ~Oppenheim sign - applying pressure to the medial side of the tit Meuse Ce jexion oF The Woes induced by rapid Sy Neurology Simplified Causes of absence Pyramidal lesions J I deformity; especi eformity; especially hh that the joint ca) activation, ~ Severe HNL weakness (Power less than grade 2). senate less tha . tncompicie pyrainidal Syndrome: If the fibers which innervate dorsiflexor muscles of the foot are not involved, = Spinal shock: In ai of Jespil allux valgus such n't go up, although EHL ile spinal shock no response Tight be seen from plantar stimulation due to . depressed spinal segmental pctivity. | | seh: -- 2 Mpa Chee ike Fesp : why Opiads Bee longus tendon, Sv er2- f the extensor hallucis Taleet doaselt percussion of the dorsum of the fool. percussion on the tips of the Beisasie’s Qeltex —> TEL conden (Mintmel bakin) What ts pseudo Babinski sign? In cases of hyperkinetic movement disorders like striatal toes ( ) and choreo-athetosis; there Of great toes; mimicking the erentiated from true Babinski reflex by absence of contraction of Hamstring: tibialis anterior and tensor fascia Tata muscles and also pseudo Babinski can be inhibited by pressure over the base of the great toe. Patient has difficulty in flexing the hip, knee and ankle since flexor muscles are weak in the lower limbs and tone is increased in the anti gravity muscles. Patient therefore drags the foot. The foot is raised from the ground by tilting the pelvis and from the hip, so the foot tends to describe an arc, the little toe scraping along the floor. Upper arm adducted and flexed with minimal swing of shoulder; elbow and wrist flexed. HISTORY TAKING IN A PATIENT WITH HEMIPARESIS Motor symptoms © Decreased movements - Paresis/paralysis © Increased movements; involuntary movements Feeling of stiffness or heaviness in limbs/History of dragging of lower limb while walking © What to ask ? = Upper limb: Difficulty in using a pon, using comb/ooth brush, buttoning-unbuttoning the shirt, difficulty in raising arms above the head. OO eee Scanned with CamScanner. Neurology Simplified = Lower limb: Difficulty to lift the foot in front D. Time of the day at onset of symptoms - of the other and difficulty in walking, knee ¢ During sleepfearly morning hours - buckling, difficulty in walking upstairs/ thrombosis downstairs. «Day time - hemorrhage or embolism + Trunk: Difficulty in turning in bed, getting After exertion - hemorthage up from the supine position. = Face: Angle of mouth deviated to the Other Symptoms to ask opposite side, unable to whistle ete. ¢ Headache, vomiting, altered sensorium : Indic re systemic hypertension. Sensory symptoms Symptoms of raised ICP : Headache, vomiting, blurring of vision or transient visual obscuration (TVOs) Symptoms of other systems like palpitation, chest pain and dyspnea + Reduced sensations - hypoesthesia/anesthesia Increased sensation = Occurs in Thalamic stroke where threshold * for pain is increased. = Spontaneous, diffuse, unpleasant or burning pain, exacerbated by touch Importance of history of headache in stroke (Dejerine-Roussy syndrome) «Severe headache accompanying paralysis: Subarachnoid hemorrhage, intracerebral History of Higher function disorders hemorrhage and hypertensive encephalopathy * Altered consciousness © Language disturbance * HemineglecVagnosia + Mild to moderate headache accompanying paralysis: Cortical venous thrombosis, posterior circulation stroke. Severe neck pain or occipital pain accompanying paralysis: Carotid or vertebral Cranial nerve Disorders . © Especially VII cranial nerve. Onset - sudden or insidious Sudden onset indicates vascular or traumatic etiology (Rarely demyelination). Headache preceding paralysis for weeks or months: Subdural hematoma. SOL (Space occupying lesion), CADASIL (Usually history of migraine preceding many months to years) B. Progress ‘Slat + Headache following paralysis: May suggest . ee ICP in stroke patients due to mass effect. B ‘+ Progressive with subsequent amelioration . ae © Rapidly progressive Cpe Importance of seizures history in stroke Suiltering + Seizures just prior to or accompanying * > rain lysis: Embolic stroke, cortical venous - Traumatic lesions are stationary: do not Baralysis: be dating aromas thrombosis, aypertensive encephalopathy = Vascular lesions progress initially and * Seizures followed by paralysis: Todd's then start ameliorating. paralysis, SOL or hypertensive encephalopathy. - Carotid hemiplegia is stuttering in © Seizures are uncommon in lacunar infarcts or progress (step ladder pattern). subarachnoid hemorrhage. C.. Rapidity of development of the symptoms i + Rapid in cerebral hemorrhage and embolic ake Vascular (Ischemic and hemorrhagic} Complicated Migraine Todd's pal Hypoglycemia Multiple Sclerosis, ADEM Mitochondrial disorder (MELAS) Hysterical hemiplegia a Stuttering or relatively slow in thrombotic stroke, ‘* Rapid onset with relentless progression in cerebral hemorrhage. Over few hours or days seen in infective or demyelinating disorders, Scanned with CamScanner“A, Elderly + History of hypertension, diabetes mellitus, Ischemic heart disease, Hypercholesterolemia, acute myocardial infarction, + Embolic source (cardiac, artery to artery), arteritis/vasculitis etc B. Young adults or children 1. Cardiac diseases - Rheumatic valvular heart disease - Congenital heart disease ~ Patent foramen ovale + Cardiomyopathy 2. Cerebral arteriopathy Takeyors CodMoys dt? + Focal cerebral arteriopathy + Moyamoya disease/syndrome tion of arteries BARRA Pet eet 3. inféétions > Meningitis (ubercular/fungal) = Varicella 2 4. Hematologieal” > Hypercoagulable states (antiphospho- lipid antibody syndromes, d iciency of antithrombin II or protein § or C, resistance to activated protein C) + Leukemia Sickle cell anemia > Disseminated intravascular coagulation - Thromb > Polycythemia ~_ Thrombotic thrombocytopenic purpura 5+ Gandhi te crendiels Cacunc) Neurofibromatosis ‘Type 1 Homoe 6° Ora recent delivery - (cvr 24 fester 7 Spllagon vascular ose et 7 —~Th GENERA, EXAMINATION Pulse. strregular pulse Cardio-embolic stroke or Absent pulsations from some arteries ‘Takayasu arteritis (Upper limb pulses unequal or absent) Giant coll arteritis (Superficial temporal artery pulse absent) H/o /E lima 4 bolaydlet. Neurology Simplified Artery to artery infarct (Absent or feeble carotid artery pulsation) * Low volume pulse Hypovolemic state and hypoxic brain injury. Suggest atherosclerosis, « Rigid/thickened radial artery on palpation + High volume pulse/ dicrotic pulse/ pulsus bisferiens Rheumatic valvular heart disease. Blood pressure Hypertension : Important risk factor for ischemic as well as hemorthagic stroke. Unequal blood pressure in upper limbs suggests ‘Takayasu arteritis or subclavian steal syndrome, 1 is better to record blood pressure from non- paralysed limb to avoid low BP recording due to vasomotor paralysis on paralysed side, > With 10 mm rise in mean blood pressure risk of stroke is increased by about a 30%, Carotid artery examination in stroke patients * The carotid arterial pulses are usually examined with the patient supine and the neck turned to the opposite side. The patient's chin should be elevated to allow easy palpation and yet not enough to tighten th muscles. * The fingers should be positioned between the larynx and the anterior border of the 1 muscle at the level of the cricoid cartilage (C, vertebra). + Palpation of the carotid artery normally detects @ smooth, fairly rapid ouiward movement beginning shortly after the first heart sound and The pulse peaks about way through s: of carotid pulsation ise in carotid pulse amplitud inequality between th plitude two usually sug) athe possible causes include ection, arteritis, or embolus. The | marked dec carotid obstruction or may be transmitted from. a cardiac murmur, CAROTID BRUIT Carotid bruits generally result from turbulent, non.” Jaminar flow through a stenotic lesion, which causes arterial wall vibrations distal to the stenosis, The Scanned with CamScannerNeurology Simplified vibrations are Lransmitted to the body surface, where they can be detected with it How to examine for bru mine patient in a quiet room, in a relaxed and comfortable position. Use the diaphragm of th stethoscope, because it detects the higher frequ sounds of arterial bruits better than the bell. Ask patient to breathe in and hold breath. Listen over an area beginning from just behind the upper end of the thyroid cartilage to just below the angle of the jaw. icant bruit Bruits at the bifurcation of the common carotid artery are best heard just below the angle of the mandible. At this level the common carotid arte Difurcatés and gives rise to its internal carotid artery. Diffuse bruit over neck or bruit radiating to the base of the neck is nota very specific indicator of internal carotid artery disease. Bruit localised only at the bifurcation is more specific for internal carotid artery origin stenosis. On asking the patient to perform Valsalva maneuver, internal carotid bruit may decrease, while external carotid bruit tends to Degree of carotid stenosis and bruit With modest arterial stenosis (< 5096) or irregularity, bruit will be of short duration and heard just in mid- systole. As the degree of stenosis increases, the bruit becomes more audible and longer. The long duratio: high frequency bruits represent_ haemodynamically severe carotid stenosis. The intensi correlates with the degree of stenosis to some extent. A harsher bruit implies greater stenosis, bul remember that stenosis of more than 90% may be associated with low flow through the carotid artery and hence no audible bruit at all, Other causes of noises in the neck Bruits transmit as we move the stethoscop the angle of the jaw rated towards jateral and more obviow Thyroid bruits are bil y Tocated over the gland. A hyperdynamic circulation tends to cause a diffuse and bilateral bruit Venous hums are caused by flow in the interna “jugular vein, are continuous and roaring & are obliterated by light pressure over the ipsilateral jugular vein. ~ Massiv An arterial bruitin the supraclavicular fossa suggests either subclavian or proximal vertebral arterial, disease, bul a transmitted bruit from aortic stenosis must also be considered. On increasing blood pressure cuff pressure above systolic, vertebral bruit increases, while the subclavian bruit decreases.” CNS EXAMINATION HIGHER FUNCTIONS Consciousness Orientation Memory Language Speech Frontal or parietal lobe signs Presence of hallucination/del jusion/illusion, + Level of altered sensorium - Drowsy - Easily arousable. - Stuporous - Not easily arousable. = Semiconscious - Responding to painful stimuli only = Unconscious - No response to even painful stimuli Enumerate causes of altered sensorium with hemiparesis? Cerebral hemorthage/Bleed cerebral infarct. Brain stem infarct. CVT with hemmorrhagic infarct. using epidural or subdural hematoma, nated encephalomyelitis (ADEN. ing lesion: tuberculoma or cerebral Space absce: Enumerate causes of stroke with impaired orientation? Thalamic stroke involving nucleus. Frontal lobe infarcts (Hyperactivity, confusion, akinetic mutism). Enumerate causes of stroke with impaired Stroke associated with sudden onset memory loss is seen with strategic infarcts. © Thalamic stroke involving anterior or dorso- median nucleus. . Posterioi artery infarct causing medial temporal (hippocampus) involvement. * Sometimes caudate nucleus infarct Scanned with CamScanner_ lulti-infarct state (vascular dementia) is common cause of dementia; usually associated with memory impairment with behav palsy and parkinsor How the languag 1 problems, psoudobulbar signs. affected in stroke and which are the arterial territories affected? Broca's aphasia: Left MCA (Superior division) infarct; usually associated with right hemiparesis. Wernicke's aphasia: Left MCA (Inferior division) infarct; usually not associated with hemiparesis, but may be associated with hemianopia. Global aphasia: Left MCA stem or ICA (Internal carotid artery) infarct. Anomic aphasia: Left_angular gyrus infarct (distal branch of inferior division of MCA territory infarct) Conduction aphasia: Only repetition is affected and site of lesion is left perisylvian area; mostly oft perisylvian are due to hemorthage. Does subcortical infarct cause aphasia? ~ Infarct involving thalamus and basal ganglia; especially on left side can lead to aphasia. is speech affected in stroke? 's common because of facial palsy. Dysarthri Sometimes bilateral pyramidal fibers are affected in infarct leading to spastic dysarthria, Lesion involving cranial nuclei IX and X can lead to nasal intonation due to paralysis of palatal muscles. CRANIAL NERVES Important cranial nerve deficits in hemiple; Papilledema (Il). Plosis and abnormal/asymmetrical pupils (Ill). Abnormal eye position (Ill, IV, VI), conjugate iation of eyes. ial droop and dysarthria (VI). Dysphagia and nasal intona (1X; X). Dysphonia or hoarseness of voice (XI). 1 of speech Neurology Simpli ied UMN palsy of VII nerve : lesion above Pons LMIN palsy of VIL nerve crossed hemiplogig. Lesions al pons _ Hemiplegia without 7th cranial neryy involvement is suggestive of lesion below Pons. Eye examination in stroke patients: Papilledema can be seen in raised intracra pees gm with intracerebral bloed and massive cerebral infarcts. Tubercular meningitis with hemiparesis (due to the vasculitis) can have optic atrophy or papilledema. Qculomotor_nerve_involved_in_ Weber's syndrome, Pinpoint pupils aeseen in pontine hemorthage, | eye field infarct : Contralateral gaze : Ipsilateral gaze palsy. Discussed previously. SENSORY SYSTEM Hemi sensory loss can occur in thalamic infarct ifivolving dorso-lateral part. Cortical lesions involving association sensory cortex can lead to cortical sensations impairment _ Subcortical infarct (corona radiate, internal capsule) or involving primary sensory cortex can cause hemi loss along with hemiparesis. Post-thalamic pain syndrome (Dejerine-Roussy pontaneous pain in hemi-body ion following thalamic infarct. CEREBELLAR SYSTEM Cerebellar ata can be seen in Cerebellar infarct + Posterior inferior cerebellarartery oranterior inferior cerebellar artery infarct : Usually associated with other brain stem signs. uperior cerebellar artery infarct : Can present with pure cerebellar ataxia, uperficial anterior spinal artery infarct : Due fo fronto-ponto-cerebellar fibers affection. = Ataxic hemiparesis : capsule or basis pontis infarct. Scanned with CamScannerNeurology Simplified bellar bleed = Usually involves s riot cerebellar artery. - Common site of hypertensive bleed. EXTRAPYRAMIDAL SYSTEM * Bradykinesia, rigidity ganglia infarct. Vascular parkinsonism has been described with multiple infarct state characterized by L-dopa unresponsive lower body parkinsonism with pseudo-bulbar pals and cognitive impairment, ‘an be seen in basal ‘¢ Hyperkinetic movement disorders are common with stroke. Seen with contralateral caudate stroke, - Hemiballismus: Seen with contralateral subthalamic stroke. - Rubral tremors: Seen with midbrain stroke involving red nucleus. OTHER SYSTEM EXAMINATION © Cardio vascular System Examine for signs of congenital, valvular, ischemic and hypertensive heart diseases. + Respiratory system Examine for tuberculosis and bronchogenic carcinoma. + Gl system Examine for hepatic mass or metastasis. HIGH YIELDING FACTS What are the possible sites of lesions in hemiparesis? Cortex Corona radiata Internal capsule Brain-stem : Midbrain, pons and medulla Spinal cord Cortex Negra - ACA + Face + arm > leg 8 foley a if dominant hemisphero and hemineglect if non-dominant hemisphere involved. . is common. . nay be seen, (VeZiehed Corona radiata and subcort are present. -al white mater (Siete) focal neurologi joparesis or hemiparesis, 24 hours, © Usually seizures, headache and aphasia tend to be absent Internal capsule © Most common site affected in stroke patients. Most common cause is lacunar infarct. . ‘as corticospinal fibers are © Hemianopia may be present. Brain stem Ipsilateral cranial nerve palsy with contralateral hemiparesis * 5 D's: Associ ysarthria ted clinical features = Disequilibrium (ataxia) - Dizziness - Diplopia - Dysphagia/dysphonia © Pin-point pupil, Paralysis and Pyrexia (3P: Pontine hemorrhage) Spinal cord i (pain and temperature loss} What are the differences between congenital/ infantile hemiparesis and acquired/adult hemiparesis? Following are the features of hemiparetic cerebral palsy (congenital hemiparesis) . ymmetric Moro reflex © Early handedness ler limb / hand (compare nail and thumb size) Delayed motor m © Higher chances of seizures lestones DEFINITIONS «© STROKE Sudden occlusion or rupture of cerebral arteries oF veins resulting in focal cerebral damage. and clini neurological deficits. OR deficit lasting more than uroimaging evidence of ablished vascular terr Tiniead See of Ae with 1 abnormality in an 1 Scanned with CamScannercs ‘TRASIENT ISCHEMIC ATTACK (TIA) Classic definition of TIA Sudden, focal neurologic deficit lasting < 24 hrs Presumed to be of vascular origin = Confined to an area of the brain or eye porfused by a specific artery OR New Definition of TIA = ATIA is a brief episode of neurologic dysfunction caused by focal brain or retinal ischemia, with clinical symptoms typically lasting less than thour, and without evidence of acute infarction. ABCD2 score: Used in TIA patients to predict risk of stroke or recurrent TIA. Age 60 or older + 1 point Blood pressure > 140/90 mmHg - 1 point Clinical - Unilateral weaknes: + 2 points > Speech impairment = 1 point Duration - 60 minutes or more - 2 points ~ Less than 60 minutes = 1 point Diabetes > 1 point 90 days risk of stroke Score <2 = 0.4-1% risk; 69% risk and « ISCHEMIC PENUMBRA ~ Ischemic tissue potentially destined for pically results; when blood flow drops below 20 mlJ/100 g/min, - In penumbra, brain cells are marginally perfused and metabolically unstable and ean be salvaged once blood supply is restored. * LACUNAR INFARCT > Small (usually 0.2 to 15 mm in diameter, 15-20 mm are mega-lacunes) noncortical infarcts caused by occlusion of a sin penetrating branch of a large cerebral artery, ‘These branches arise at acute angles [rom Neurology Simplified, the large arteries of the of the middle cerebral arte basilar artery. - Most_common site is putamen followed by periventricular deep white matter, = Most important mechanisms Je of Willis, stom (MCA), oF the are = Most important risk factor is hypertension, BLOOD SUPPLY OF BRAIN Branches from ICA + Hypophysial arteries: further splits into - Anterior hypophysial artery: Supply hypothalamus. The anterior hypophysial artery breaks into capillaries forming the hypophyseal portal veins which convey hormones from hypothalamus into ante: + Posterior hypophysial artery: Supply to neural lobe of the pituitary * Ophthalmic artery: Supply retina and optic nerve. © Posterior communicating artery: Runs backward to join the posterior cerebral artery ‘© Anterior choroidal artery: Supply choroid plexus of temporal horn of lateral ventricles and optic tract, lateral geniculate nucleus and lower half of posterior limb of internal capsule. © Middle cerebral artery: branches off frontal, parietal and temporal branches supplying primary motor and premotor cortex, frontal eye field, primary somatosensory area. Left middle cerebral artery supplies language center. © Anterior cerebral artery: Meets together to form ior communicating artery before they join. off recurrent artery of Heubner, also called al straite arlery, supplies corpus striatum. It then ascends along the longitudinal Tissure en bends backward around the genu of the corpus callosum. It supplies to leg and bladder area and corpus callosum, Branches from vertebro-basilar system Vertebral artery, branch from the subclavian artery. joins together to form the basilar artery. The latter artery splits into posterior cerebral Branches of the vertebral artery * Anterior spinal artery and posterior spinal artery’ supply to spinal cord, Scanned with CamScannerNeurology Simplified «Posterior inferior cerebellar artery (PICA) largost branch of vertebral artery supplies postero: lateral medulla, cerebellar hemisphere and inferior vermis. Branches of basilar artery © Antorior inferior cerebellar artery (AICA) supplies inferior surface of the cerebellum and postero-lateral pons. * Labyrinthine artery supplies the membranous labyrinth of the internal ear. Lateral ventricle Caudate \ Internat capsule / Globus Pallidus Hippocampus —— ‘Temporal lobe aa, © Pontine arteries supply pons and pontine tog © Superior cerebellar artery supplies pons, superior cerebellar peduncle and inferior colliculus, ete { % Posterior cerebral artery t «Supplies to the occipital cortex, posterior parietal and medial temporal lobe. Also supplies to postero-lateral thalamus. E Fig. 3. Showing parts of brain and their blood supply Circle of Willis, + Consists of : > Anterior communicating, anterior cerebral, internal carotid (short segment), posterior communicating and posterior cerebral arteries. Normally not too much blood flow, could be served as alternative route if one of the arteries is occluded. * Common site for aneurysms ~ Terminal part of internal carotid artery, anterior communicating artery and proximal part of middle cerebral artery. anteror cerebsal anny communicating arte) portenor conmuncath@ ‘tery supenor cerebeliar artery asia artery anterior infor Gerebear artery ventral ary postenor infor (arbor anery Aig. 4. Circle of Willis Scanned with CamScannerNeurology Simprig — Describe various clinical findings in anterior, middle and posterior cerebral artery strok ight face and arm weakness # Nonfluent or Broca’s aphasia farct A superior division ensory loss of UMN Left MCA inferior divisions infarct © Fluent, Wernicke's aphasia © Right visual field deficit } (Motor findings are usually absent) Left (or right) MCA deep territory © Right pure motor hemiplegia (lenticulostriate arteries) © Ataxic hemiparesis «Right hemiplegia # Right hemisensory loss © Right hemianopia © Global aphasia (Left gaze preference due to frontal eye field lesion) Right MCA superior di sions infarct © Left hemiparesis, © Left hemineglect Right MCA inferior division infarct Profound left hemineglect + Left visual field deficit Anterior choroidal artery infarct + Left hemiplegia (Jemporal heen of Ratirsd vendeicle (3-H syndrome) + Left hemisensory loss ¢ frre Inol- of fost inletnal capsid), Most common artery damaged by + Left homonymous hemianopia ( talexaS gemeate mucin) neurosurgical intervention. Small infarct: BIG deficit Left ACA infarct «Right leg weakness Grasp reflex and frontal lobe behavioral abnormalities *Transcortical motor aphasia Right ACA infarct * efi leg weakness * Grasp reflex and frontal lobe behavioral abnormalities © Left heminegleet +/- LefvRight PCA infarct © CiL homonymous het ianopia + Extension to the splenium of corpus callosum can cause alexia without agraphia (on left side) © Thalamus involvement may result in aphasia, hemisensory loss, disorientation, ataxia etc, Bilateral PCA infarct may results into the Anton's tical blindness; visual agnosia, AL Scanned with CamScanner