Week 3 Central Nervous System Learning outcomes 1 Anatomy,physiology of cerebral cortex,brain stem,cranial nerves,Spinal cord and peripheral nervous system. 2.Student must have knowledge of ascending and descending pathways; and clinical problems associated with lesion of these pathways. 3 Students must be able to localise site of CNS lesions 1 Cerebrovascular disease : elderly/young patient 2 Brain stem lesions – midbrain,pons,medulla 2.Cranial nerves : 3rd nerve’ , facial nerve 3. Spinal cord disease 4 Cerebellar lesions 4 Peripheral nerve lesions 5 Meningitis/encephalitis 6 Headache Problem 1 A 60 year old patient presents with sudden onset of left sided weakness and slurring of speech. ( ) dysarthria Q.Take a relevant history from this patient. - orthopnea - PND * endogan ● Left-sided weakness: ○ Onset: sudden/insidious ○ Duration ○ Site: upper limb/lower limb/both ○ Affected limbs are spastic or flaccid ○ Associated symptoms: headache, nausea & vomiting, blurring gxqflseeaxed ' of vision, facial asymmetry/dribbling of saliva, sensory loss, vision defects (reduced acuity/visual field) ○ Progression: rapid or slow ○ Ability to walk, carry out normal routines ● Slurring of speech: upper motor neuron facial nerve palsy ○ Onset, duration ○ Expressive dysphasia/receptive dysphasia/dysarthria ○ Associated symptoms: dysphagia, choking ● H/o balance problems, loss of consciousness ● H/o fever, trauma ● Past history: DM, HTN, dyslipidaemia, hypercholesterolaemia, prosthetic valves, arrhythmia, previous same episodes, previous h/o MI, stroke, any medication (aspirin/warfarin) ● Personal history/risk factors: smoking, alcohol, obesity ● Family history: DM, HTN, hyperlipidaemia, MI, stroke - . { ● Handedness: dominant hand etc Previous hx -Lower limb: Ant cerebral artery lesion -Upper limb: middle cerebral artery lesion * Differential diagnoses: • social ↳ how the pro recovered ↳ medication history Expressive dysphasia is a difficulty in expressing what you want to say. This may be in the form of speech but may also affect their writing and reading aloud abilities. Speech may be non-fluent, and a person may find it difficult to find the right word for something. Receptive dysphasia is when a patient has difficulty with the understanding of written or spoken language. Patients can both hear and see the words but not process and make sense of them. Dysarthria is a motor speech disorder in which the muscles that are used to produce speech are damaged, paralyzed, or weakened. The person with dysarthria cannot control their tongue or voice box and may slur words. There are strategies to improve communication. µ expressive aphasia motor aphasia cannot ↳ patient express himself sensory aphasia CReceptive) ↳ pro cannot express - homsaf Dysphonia ↳ pt cannot - talk loudly ↳ vocal cord problem globus aphasia - cannottalk cannot Q.State the expected examination findings. General examination ● Level of consciousness: GCS score ● Pulse : irregular rhythm (atrial fibrillation) ● BP: high ● Face: facial asymmetry, dribbling of saliva on left side ● Eyes: homonymous hemianopia (optic radiation involvement) ● CVS: Carotid bruit, JVP, murmurs (source of embolism) ● RS: signs of pulmonary oedema or infections ● Leg: pain and swelling (usually unilateral in DVT) ● Gait: hemiparetic gait hemiplegia gait CNS examination ● Higher mental functions: express - Judgement ○ Consciousness: alert and conscious, GCS score (14/15) ○ Orientation: well oriented (time place person) Ahistorical event ○ Memory: immediate, recent and remote memories are intact ○ Intelligence: intact Count / simple maths) ○ Speech: dysphasia/dysarthria , . , ● Cranial nerve: do facial nerve , glossopharyngeal nerve [ (swallowing problems) ] ● Motor: ○ Trophic changes: loss of hair, brittle nails, cold, shiny & dry limbs ○ Unilateral (left) weakness (hemiparesis)/hemiplegia ○ Hypertonia of muscles (UMNL) The Hoffman sign is an involuntary flexion ○ Decreased muscle power of affected limbs movement of the thumb and or index finger when ○ Muscle wasting – no since it’s a UMNL , wasting common in the examiner flicks the fingernail of the middle LMNL finger down. The reflexive Hemiparesis is a mild or pathway causes the thumb ○ Pronator drift (left) partial weakness or loss of to flex and adduct quickly. strength on one side of the ○ Tendon reflexes: hyperreflexia (UMNL) body. Hemiplegia is a ^ severe or complete loss of ○ Hoffman sign strength or paralysis on one side of the body. ● Sensory: ○ Unilateral (left) hemiparaesthesia/anaesthesia ○ E.g. : touch, pain, vibration, temperature ○ Loss of proprioception ○ Babinski’s sign: +ve on left side (UMNL) ● Optic nerve exam: visual field- homonymous hemianopia (since optic radiation is affected) ● Check ankle clonus is a rhythmic, oscillating, stretch reflex, the cause of which is not totally > Clonus known; however, it relates to lesions in upper motor neurons and therefore is generally accompanied by hyperreflexia. ● Gait : hemiparotic gait- hip, knee, ankle extended, upperlimb flexed, circumduction CVS and RS exam: cannot swallow p patient (aspiration pneumonia)g - RS: crackle in right side of lung (since right bronchus is straight) - CVS: carotid bruit in carotid artery in neck both sides, atrial fibrillation, murmurs , BP Q. State the investigations that you would do. ● CT scan of head- confirm site of lesion, extent of brain affected ● FBC - exclude anemia, polycythemia, thrombocytosis ● Blood sugar - exclude hypoglycemia/DM ● Blood urea and serum creatinine - to know hydration status ● Serum lipid profile ↳ to rule out renal failure ● Serum electrolyte ● Chest X Ray → cardiomegaly ● ECG → to rule out arrhythmias , hypertrophy I left ventricular) , mi ● Echocardiography in suspected cardioembolism: C Atrial fibrillation – atria cannot contract properly , so thrombus formation in atrium,, left ventricular hypertrophy ● Carotid duplex Ultrasound to identify extracranial vessel disease ● Transcranial Doppler Ultrasound to identify intracranial vessel disease ● MR angiography (MRA) or CTA of cerebral vessel CT scan of patient is shown: F- Rt . Ventricle compressed Q Describe the radiological findings. ● Hypodensity of right cerebral hemisphere – cerebral infarct (due to ischemic stroke) ● Swelling and compression of right ventricle with midline shift to the left ● Loss of grey white matter differentiation ● Massive right-sided cerebral infarction Q State the likely diagnosis Cerebrovascular Accident (ischaemic stroke) with left sided hemiplegia Q. Mention the underlying pathogenesis of this clinical problem. Ischemic stroke is due to sudden occlusion of an intracranial vessel with reduction in blood flow to the brain area supplied by that vessel. Occlusion happens either due to in situ thrombosis (atherosclerotic vessel) or embolus from a distant site (internal carotid and aortic arch) Three main causes of ischaemic stroke are: ● Atherothromboembolism (50%) ● Intracranial small vessel disease (penetrating artery disease) (25%) ● Cardiogenic embolism (20%) plaque ruptures → Thrombi embolic event Other causes include arterial dissection, trauma, vasculitis (primary/secondary), metabolic disorders, congenital disorders and other less common causes such as migraine, pregnancy, oral contraceptives, etc. Acute occlusion of intracranial vessel > Reduce blood flow to the brain region it supplies > Ischaemia/Infarction depend on severity of reduction of blood flow. If blood is restored before significant amount of cell death, patient may experience only transient symptoms (Transient Ischaemic Attack). The infarcted area is surrounded by ischaemic areas (ischaemic penumbra) where if blood flow is restored within reasonable time, the changes are reversible. If blood flow is not restored, it will eventually undergo infarction (irreversible cell death). Biochemical changes: Hypoxia > Mitochondria cannot produce ATP > Failure of membrane pump > Cytotoxic edema and membrane depolarization > Calcium enter cell and glutamate is release from synaptic terminals > Glutamate lead to intracellular calcium accumulation > Excess calcium inside neurons produces free radical by membrane degradation and mitochondrial dysfunction > Death of neuronal cell Q. Outline management. Admit to multidisciplinary stroke unit General measures: 1. Assess airway, breathing and circulation. 2. Ensure clear airway. Keep the patient nil by mouth. 3. Give oxygen by mask if low saturation. 4. Monitor BP and pulse. Do not treat HPT if SBP is < 220mmHg or DBP < 120 mmHg. Mild HPT is desirable at 160-180/90-100 mmHg. BP reduction should not be drastic. 5. If dehydrated, give fluids parenterally. 6. Assess nutritional status. If dysphagia persists, feed via nasogastric tube. 7. Monitor blood glucose. Treat hyperglycemia with insulin and hypoglycemia with glucose infusion 8. If patient has fever, investigate and treat the causes. Give antipyretics 9. Regular change of posture to avoid bed sores. 10. Care of bowel and bladder to avoid infection. 11. Control Hypertension/DM/Dyslipidemia. 12. If patient develops cerebral edema, give IV mannitol 0.25-0.5 g/kg and head end elevation. 13. If hydrocephalus is present, drainage of cerebrospinal fluid via an intraventricular catheter 14. Hemicraniectomy and temporal lobe resection if infarction is very large Ateplase? Specific treatment (Reperfusion): ¥ " T 1. Intravenous Thrombolysis: Intravenous rt-PA (0.9mg/kg, - maximum 90mg), with 10% of the dose given as a bolus followed by a 60-minute infusion, is recommended within 4 hours of onset of ischaemic stroke. IV rt-PA is given only if there is a physician that expertise to manage stroke, availability of appropriate neuroimaging test, and can manage complication of thrombolysis (intracranial hemorrhage) The main contraindications are bleeding risk (recent haemorrhage, anticoagulant therapy), delay to treatment, high BP >185/110mmHg, recent major surgery, prior stroke or head injury within 3 months, GI bleeding in preceding 3 weeks 2. Antithrombotic treatment: Start aspirin within 48 hours of stroke heparin [ onset. Use of aspirin within 24 hours of rt-PA is not recommended. If thrombolytic is contraindicated, give 300 mg/day of aspirin 3. Anticoagulant (Heparin and LMWH) not routinely recommended 4. Endovascular techniques: Intra-arterial thrombolysis and endovascular thrombectomy 5. Rehabilitation: Early physical and speech therapy embolic or isheemic → Thrombohsse stroke? thrombotic → aspirin * embone stroke : Long-term management: ↳ heparin - . 1. Address the RF (HPT, Smoking, Obese, DM, Alcohol) 2. Antiplatelet: Aspirin 75mg-325mg daily 3. Heparin is given if there is AF 4. Anti-HPT: ACE-inhibitor or ARB 5. Lipid reduction with simvastatin 40 mg 6. Control blood glucose level 7. Stop smoking and reduce alcohol intake 8. Carotid endarterectomy if internal carotid artery stenosis >70% Discuss lobes in cortex and cerebral function of different cortical centres Lobe Normal Function Frontal Lobe Personality, Emotional response, Social behaviour Parietal Lobe Dominant side: Calculation, Language, Planned movement, Stereognosis Non-dominant side: Spatial orientation, Constructional skills Temporal Lobe Dominant side: Auditory Function, Speech, Language, Verbal Memory, Olfaction Non-dominant side: Auditory function, Music, tone sequences, Non-verbal memory (music, faces), Olfaction Occipital Lobe Analysis of vision *NOTES: Types of stroke: 1. Ischaemic stroke (82%): a. Thrombotic b. Embolic An ischemic stroke is when blood vessels to the brain become clogged. A hemorrhagic stroke is when bleeding interferes with the brain's ability to function. A stroke is a medical condition where there is an interruption in blood flow to the brain. 2. Haemorrhagic stroke (15%): a. Intracerebral b. Subarachnoid (rare:3%) Risk factors: 1. Diabetes 2. Hypertension 3. Obesity: hyperlipidaemia 4. Smoking 5. Alcohol Causes of stroke: Old patient Heart diseases E.g.: Atrial fibrillation, valvular disease, IHD Hypertension, diabetes Atherosclerosis Trauma Problem 2 Young patient Infective endocarditis Rheumatic heart disease OCP intake SLE: vasculitis Atrial fibrillation, prosthetic valves Tuberculosis Berry aneurysm Trauma Q.Interpret this CT scan D) ✗ → Hemorrhagic stroke on right hemisphere -Bright white area – hyperdense area on the right hemisphere on frontal area -Midline shift to the left -irregular margins -cerebral edema – around the hemorrhage Q.Mention the clinical presentation of these patients. -Sudden onset of severe headache, vomitting, loss of consciousness -Sudden onset left sided hemiplagia/hemiparesis -May be associated with slurring of speech -Mental confusion Q.State the complications of stroke -Epileptic seizures -Recurrence of stroke -Dvt/ pressure sores (immobile) -Depression, anxiety -Intracerebral hemorrhage -Hydrocephalus -Pulmonary embolism - Aspiration Pneumonia -UTI -Cerebral edema -Contractures (not exercising) Q.Outline management. -Surgical removal of hematoma if severe -Nursing management (turn patient every 2 hours to prevent bed sores) -Management of risk factors : ACE inhibitors, CCB, Beta blockers for HTN, control glucose for DM - -No anticoagulants/antiplatelets → physiotherapy causes bleeding - HTN and bradycardia (Cushings reflex), nausea vomiting, headache (increased ICP) - cerebral edema à give IV mannitol (end organ damage – hypertensive emergency) f Gcs → unequal pupils → herniation side ②ilatiof @ herniation) on brain Q.Describe in brief anatomy and blood supply of cerebrum. Ant & Medial Cerebral artery : Frontal and temporal lobe Verterobasillar system : Occipital lobe, midbrain, cerebellum Communicating arteries : Left and right hemispheres Q.Describe Cushing’s reflex. -Blood flow to the brain is directly related to cerebral perfusion pressure (CPP) -CPP = Mean Arterial Pressure(MAP) - Intracranial Pressure (ICP) -Therefore MAP must be greater than ICP for perfusion of the brain -When MAP is lesser than ICP the hypothalamus activates sympathetic nervous system causing peripheral vasoconstriction and an increase in cardiac output -As a result of the increased arterial pressure, the baroreceptors in the carotid bodies are stimulated slowing the heart rate down to bradycardia. -Known as Cushings reflex/ CNS ischemic response/ Vasopressor response - Cushing Triad : Presence of HTN ( increase systolic, decreased diastolic), Bradycardia and irregular respiration in patients with raised ICP. Irregular respiration is due to reduced perfusion of brainstem or possible brainstem herniation after cerebral quelling event → T ICP compress ) vessel Q.How would you grade a comatose patient? → t perfusion t Sym I Uasocmt : 6 Q.List the differences between Upper and Lower motor neuron lesions. Q. Discuss lobes in cortex and cerebral function of different cortical centres Localisation of lesion Problem 3 [ Q.A 70 year old patient presented with right sided weakness of 3days duration.He was able to comprehend but able to speak only few words. Where is the lesion? Explain with diagrams Site - Left sided frontal lobe atthe pre central gyrus Global aphasia: Wernicke + Broca . - ( (fluent comprehend repeat) Wernicke’s aphasia: Sensory aphasia Yes (fluent) No Comprehend repeat) [Broca’s aphasia: Motor aphasia – expressive Yes Comprehend) No fflmnt No , , , Find handedness: right or left side dominance , , Problem 4 Q.A 50 year old patient presents with inability to frown on right side and drooling of saliva on right. He also had left sided hemiparesis. 1. Where is the lesion? Explain Right lower part of Pontine lesion EXPLAIN: Mouth deviated to left side, Drooling of saliva on the right,Drooping of eyelids onto right side and LMN facial paralysis 2. What is the difference between upper and lower motor neuron , repeat) ✗ ✗ i. ~ upper 31 lower damage face lower damage face ñÉÉ p¥÷ t ' e facial palsy. i Types of facial nerve palsy: UMN facial nerve palsy and LMN facial nerve palsy - If one whole half is affected: LMN nerve palsy – due to whole facial nerve or nucleus lesion - If lower half of face affected : UMN nerve palsy – corticobulbar fibres affected (upper half of face is supplied by both sides of corticobulbar fibres lower half of face is only supplied by contralateral corticobulbar fibres) LMN – contralateral facial and hemiparesis contralateral UMN – ipsilateral facial and hemiparesis Contralateral is defined as 'pertaining to the other side'. Ipsilateral is considered the opposite of contralateral and occurs on the same side 3. What is Bell’s palsy?( Explain in detail the causes you need to exclude) Acute isolated facial nerve palsy could be due to viral infection or idiopathic causing swelling of the nerve within the tight petrous bone facial canal. (Treatment: short course of steroids. ) Diagnosis of exclusion – exclude pontine lesion, Ramsay hunt syndrome, acoustic neuroma, otitis media, mastoiditis etc , then come to conclusion that it is Bells Palsy Presents with: - Unilateral LMN facial weakness Loss or altered taste on the tongue Pain behind the ear Vague altered facial sensation → Facial nerve nucleus is in the pons Niue Causes: 1. Pontine lesion is determined by: - didnt Contralateral hemiplegia (corticospinal tract) 6th and 7th nerve lesion. Ipsilateral LMNL facial nerve palsy 6th nerve palsy: lateral rectus, inability to abduct eye discuss 2. Geniculate ganglion lesion: - Ramsay hunt syndrome : reactiviation of herpes zoster virus Check for herpes zoster lesions in ear (external pinna), or rarely in throat hearing loss on affected side 4. Cerebellar Pontine Angle : known as acoustic neuroma - 5th CN µxo%Ñ 1. check for muscles of mastication ( masseter, temporalis) 2. Hyper movement of lower jaw (jaw jerk) - - 8th CN : > r 1. Reiners and webbers test, – Reiners: BC>AC , Webers: lateralising to affected side - Cerebellar lesion signs: 2. wide based gait, fall towards side of lesion, nose $ heel Shin 3. dysmetria, dysdiadokokinesia, c4. scanning speech (dysarthria) 5. nystagmus hearing loss n 1. rombergs sign, finger / conductive t muscle speech (slurring) . Weber's € pysmetria 4. Facial canal : otitis media, mastoditis – check for pus in the ear - nerve to chorda tympani: loss of taste to ant 2/3 of tongue nerve to stapedius: can’t tolerate loud sounds stylomastoid foramen : - parotid gland enlargement ( tumor) Complications of Bells Palsy: - 6 due to viral → isolated : *Treatment of Bells Patsy ↳ short courses of t.MN lesion steroid . - cant close eye and is exposed à keratitis, corneal ulcers, infection.de abrasion (close eye with eye patch throughout day, give eye drops as eyes beocme dry, surgery – lateral side of eye sew up eye become smaller - Reinervation : unwanted facial movement, abarrant innervation, while eating is tearing (tears at wrong time- due to abnormal inervation of nerves) 5. Outline origin and course of 7th cranial nerve ①- ②③④⑤⑥- ⑦⑧⑨- ④①- Nerve arises in the pons and begins as two roots: large motor root and smaller sensory root. Two roots enter internal acoustic meatus of temporal bone. Enter facial canal Two roots fuse to form facial nerve Nerve forms geniculate ganglion Nerve gives rise to: greater petrosal nerve, nerve to stapedius , chorda tympani Exits facial canal via stylomastoid foramen. Facial nerve runs ant to outer ear Gives rise to post auricular nerve Continues into parotid gland Terminates by splitting into : temporal branch, zygomatic branch, buccal branch, marginal mandibular branch, cervical branch MMC TZB - f ① ② Int Acoustic . meatus Fgf ④ temporal facial bone canal ③ ⑤ ⑥ ④ ⑦ ⑧ ① ⑨ ④ Problem 5 Q. A 40 year old hypertensive patient presents with sudden onset of unsteady gait and a tendency to fall towards the right. 1. Where is the possible site of lesion? Right cerebellum 2. What are the findings you would look for on examination of this patient. ● Gait: tandem gait test (Heel-to-Toe) is abnormal ● Cerebellar ataxia : Patient falls over when bringing feet together ● Dysmetria: overshooting of fingers in finger nose test ● Intentional tremors ● Dysdiadochokinesia: finger-nose test (inability to perform rapid, ● ● ● alternating movements) Pendular knee jerk (swinging) Nystagmus (involuntary, rapid and repetitive movement of the eyes) Scanning/ staccato speech pattern (pauses between words- British parliament ● Rebound phenomenon 3. Discuss causes. ● Posterior circulation stroke ● Tumours in cerebellum hemengiobbst ● Spinocerebellar ataxia ● Multiple sclerosis ● Post herpes zoster infection - ma , meduwblastons ● Alcohol ● Drugs eg phenytoin, carbamazepine - ● Wallenberg syndrome: ● Horners syndrome ● Contralateral spinothalamic lesion 4. Discuss anatomy and spinal tracts in brain stem.-midbrain,pons and medulla Midbrain Nim didnt discuss Right mid brain lesion : - left sided hemiplegia - right 3rd and 4th cranial nerve lesion Pons fascial nerve goes around the abducent nerve if right side of pons affected: LMN lesion - right facial palsy – fascial nerve affected - 6th right nerve supplies lateral rectus – abduct and look to right then the eye wont move due to abducent nerve lesion - left hemiplegia – pyrimidal fibers havent decessated yet Medulla - Ipisilateral 9,10,11,12 nerve palsy - Contralateral hemiplegia Spinal tracts of brainstem: Descending tract ● Pyramidal (voluntary) - Ant and lateral corticospinal (voluntary motor control of body) - Corticobulbar (voluntary motor control of head and neck) ● Extrapyramidal (involuntary motor control) - Rubrospinal - Reticulospinal - Tectospinal - vestibulospinal Ascending Tract ● Posterior column (fine touch and proprioception) ● Anterior spinothalamic tract (crude touch and pressure) ● Lateral spinothalamic (pain and temperature) – crosses to opposite side before ascending ● Ant and post spinocerebellar (unconscious proprioception) ● Spinoolivary (unconscious proprioception) Problem 6 Q. 57 year old male presents with weakness of both lower limbs for 3 months. Weakness progressively increased and patient on admission was unable to walk .Also had evening rise of temperature (suggests infection – possible TB) .No trauma.Bladder and bowel habits were normal.Patient was noted to have back pain around 10th thoracic vertebra. 1. What further examination would you like to carry out.State expected findings ● Spastic paraplegia ● Sacral loss of sensation ● Weakness of leg ● Babinski sign positive port's disease - examination: UMNL - no muscle wasting - hypertonia examine . - hyperreflexia - babinski positive - sensation: T10 compression (roughly around umbilicus so below umbilicus all sensations lost) 2. What is the likely diagnosis. ● Spinal cord compression 3. State investigations you would like to carry out. -MRI spine – show collapse of vertebra, decreased joint space -biopsy- cold abscess -for TB : mantoux test → or myehgram . -X Ray spine -Serum B12 - Subacute combined degeneration Treatment: -if compression present- decompress -Anti TB regime – INH, Rifampicin, pyrazinamide, ethambutal for arounf 1 year 4. Explain what is cauda equina and conus medullaris syndrome. Cauda equina syndrome: cauda equina bundle of nerves damaged Conus medullaris syndrome: damaged to the conus medullaris (or terminalis), at the end of the spinal cord Conus medularis : tapered lower end of spinal cord • Presentation : sudden and bilateral • Reflexes: diminished at the level, brisk below the level. (UMN) • Radicular pain : (-) less • Lower back pain: more, early • Impotence : frequent • Numbness: symmetrical • Motor strength: symmetrical , hyper reflexic, distal paralysis of lower limbs . • Sphincter dysfunction : present early both urinary and fecal inconsistence • UMN Cauda equina : bundle of nerves below the end of spinal cord • Presentation : gradual and unilateral • Reflexes: diminished because its peripheral nerve involvement • Radicular pain : + more shooting pain (due to peripheral nerve involvement) • Lower back pain: less • Impotence : absent • Numbness: Asymmetrical • Motor strength: Asymmetrical , Areflexic , paraplegia • Sphincter dysfunction : present later, only urinary retention • LMN Problem 7 Q. A 25 year old foreign worker is admitted with tingling and numbness of both lower limbs..Subsequently,it spread to the upper limbs. 1. What is the likely diagnosis? 2. State the expected examination findings. 3. State how you would confirm your diagnosis. 4. Outline management. List differential diagnosis of patients with peripheral neuropathies. a.What is the likely diagnosis. Guillain Barre syndrome- autoimmune (minimal sensory loss, generally motor loss) Hx: - how it started , spread , duration - preceeding infection - starts in lower limbs and ascends upwards fast LMN signs as peripheral nerves are involved b.State the expected examination findings. Sensory ● Distal paresthesia and pain in muscles ● More proximal part of the muscles Motor ● Areflexic*** - suspect Guillain Barre ● Facial and Bulbar weakness ● Diffuse weakness and loss of reflex µµHP0i y Respiratory weakness which can lead to respiratory failure Miller-Fisher syndrome: Internal and external ophthalmoplegia, ataxia and areflexia c.State how you would confirm your diagnosis. ● CSF- Increase protein, WBC normal (Cytoalbuminemic dissociation of CSF) 7 ● Electrophysiological changes- conduction block, multifocal motor slowing, delayed f waves Antibodies to ganglioside GM1 ● d. Outline management. Plasma exchange ● IV. immunoglobulin ● iv Ig therapy ; for 5 days at 0.4g/ ● Nursing measures to prevent bed sores and DVT ● Monitor respiratory functions, intubate if needed (patient recovers after 2-3 weeks usually) I t 90% patients recovers → Protein ↳ Lumbar T , cell Cytoalbumic puncture : count normal disassociation left lateral fetal position and insert between 13,14 DDx for Guillain Barre: Hypokalemia, polio, botulinum, myasthenia gravis, cord compression, transverse myelitis DX peripheral neuropathy isoniazid alcoholism → , , myasthenia gravis , - - - opthnnluwpluju A reflex Ataxia Problem 8 Q.A 30 year old patient presents with fever of 5 days.He also has headache,vomiting and appears drowsy. 1. What is the likely diagnosis? Meningitis 2. Discuss the different etiological causes. - photophobia , sericeous headache - Kerning budzinski , vomit , ia , 3. Mention the investigation you would do and expected results. ● CT Scan for contraindication of lumbar puncture ● Lumbar puncture for CSF (make sure no increased ICP symptoms d- – nausea, vomiting , headache, papilledema) ● Blood culture ● PCR T , =fmdÉ¢tw ↳ papiledema - → wise brain herniated blurred margins tortuous , haemorrhage , vessels * if papiledemn then Lumber Pune contraindicated 4. Explain how analysis of CSF will help you determine the etiological cause? e. Hx taking usual complaint: fever, headache drowsy, neck stiffness, altered consciousness, rash(petechial, purpura), vomiting, photophobia, focal neurological deficit. Fever: Onset and duration of fever? When does is start ( morning, evening, night) Progression (few hrs, all day, night only) + evening rise of temp + night sweats? Associating symptoms (night sweats, chills, rigor, rash, urinary complain, cough, chest pain, pain abdomen, headache, loss of consciousness, weight loss, polyarthritis) Hx of sexual exposure, sex hx, travel history? Medication taken? Headache: . Site ? Time of onset? Severity? Nature of headache? (throbbing, burning) How does it start ? How long does it persist? Recurrent? Aggravating factor ( coughing, straining, or change of posture) ? Relieving factor? Preceding by aura? Associate fever vomit weakness blurring vision vertigo nasal stuffiness, lacrimation, breathlessness? Examination : Complies encephalitis infee spreed if Neck stiffness: → Kerning sign Brudzinski sign – flex neck , knee and hip flexed → → Treatment IV penicillin (N . meningitis) 3rd gen cephalosporin co - 14 days ] herniation brain due ICP to → Vision → abscess cerebral 31 hearing septicemia Problem 9 Q.A 42 year old patient presents with left sided headaches for last 6 months.He also says that headache is associated with nausea and T loss vomiting. He has 2 attacks per week and unable to work during the headaches.Mother has similar problems. grain became familial 1. What further history would you take? 2. Discuss the differential diagnosis of headaches.Explain with reasons. 3. What characteristics of headaches warrant further investigations? 1)Further history to be taken: ● Site of headache pain: ( unilateral presents in migraine) ● Onset of headache : sudden/gradual If headache is constant or come & go? ● Character of headache( if throbbing / band-like) ● Radiation present? ● Aggravating & Relieving factors of headache: ● If patient have history of any medication, substance abuse, head trauma. ● Associated symptoms such as fever & neck stiffness, photophobia ● Triggering factors: Caffeine (migraine), stress,dehydration, excessive codeine use ● Time: Did headache changed over time? If it worsen in mornings or any particular time of the day? ● How often headache symptoms last each episode? ● Severity of headache : If headache affects daily functioning of life? ● Aura – preceding manifestation (warning sign) 80% don’t have aura same y time several for days 1 morning to noon highest - - Rhinos sheer lacrimation 2. DD ● Hereditary migraine ( without aura ) - not associated with sensory disturbance Unilateral suggestive of migraine headaches Episodic in nature and not more than twice a week Has familial predisposition of migraine from 1st-degree relative ● Tension-type headache - patient presents with primary headache symptoms No known underlying conditions or causes To rule out co-existing mixed chronic daily headache 3. (i) - lateralized and severe head pain, followed by fixed neurological deficit: arterial dissection is considered - Unilateral pain localized to the face, frontal region or eye: carotid dissection - Unilateral or bilateral occipital pain: vertebral dissection (ii) - Headache of raised intracranial pressure-type, like headache worsens on walking, exacerbated by coughing, sneezing or straining: feature of cerebral venous sinus thrombosis (in which focal signs including seizures are found) - Usual presentation: subacute raised pressure (iii) - Sudden, severe headache: subarachnoid hemorrhage (most imp symptom) - Cardinal symptom: exceptionally rapid onset, described as being ‘like a hammer blow to the head’ or ‘explosion in the head’ - Reaches maximum in a split second: is termed as ‘Thunderclap headache’ - Other symptoms: occipital localization of pain, neck stiffness, nausea, vomiting, and exertion or Valsalva immediately preceding to headache - CT scan is done to seek evidence of acute subarachnoid blood, if CT is (-) a lumbar puncture is done to look for red cells or their breakdown product (iv) - Aching, or throbbing headache exacerbated by coughing, bending over or straining, worsens in the morning and causes wakening from sleep, worsens on exertion or on lying flat - As headache worsens vomiting,diplopia, and papilloedema develop - Raised intracranial pressure(ICT): may due to obstruction of normal CSF flow by an intracranial tumour or another mechanism affecting CSF dynamics. - First clinical priority: exclude an intracranial mass lesion by imaging with CT or MRI - If there is no mass lesion, can be due to other mechanisms: - (v) - Angle closure glaucoma(acute raised pressure in the eyeball) may lead to headache, particularly around the eye, as well as visual abnormalities, nausea, vomiting and a red eye with a dilated pupil. (vi) Headache in older people, particularly when associated with visual symptoms or jaw claudication, may indicate giant cell arteritis (GCA), in which the blood vessel wall is inflamed and obstructs blood flow. Management: Sumitriptan (acute attack) , Prophylaxis: b blockers What characteristics of headaches warrant further investigations? -Stabbing headache, excruciating pain (subarachnoid hemorrhage) -Thunderclap headache -Examination: neck stiffness (suspect subarachnoid hemorrhage) -headache, vomiting à investigation required CT scan for subarachnoid haemorrhage Red flag signs: -Loss of consciousness -Paralysis of a limb -Neurological signs -< 40 is more worrying -Raise ICP -Vomiting , fever -Weight loss, raised BP -Prolonged cough with headache