Cauda Equina syndrome - Sheffield Peer Teaching Society
NEUROLOGY NEUROLOGY Phase 2A Revision Session Amogh Patil and Azhar Merchant 31/03/17 The Peer Teaching Society is not liable for false or misleading information What to cover? The Peer Teaching Society is not liable for false or misleading information TIA and stroke Aetiology
Thrombosis in situ Embolism from heart (valve disease, mural thrombus AF) or carotid (athero-thromboembolism) CNS bleed associated with HTN, aneurysm rupture, head injury Young patient vasculitis, thrombophilia, SAH Modifiable risk factors? x4 HTN, smoking, hyperlipidaemia, obesity Non-modifiable risk factors? x4 DM, male, vasculitis, hypotension The Peer Teaching Society is not liable for false or misleading information
Stroke (Bamford classification) Total anterior circulation syndrome (TACS) (large cortical stroke in ACA/MCA territories) all 3 of: Contralateral weakness (and/or sensory deficit) of face, arm + leg Homonymous hemianopia Higher dysfunction dysphasia, visuospatial disorder Partial anterior circulation infarct (PACS) (cortical stroke in ACA/ MCA territories) 2 of:
Contralateral weakness (and/or sensory deficit) of face, arm + leg Homonymous hemianopia Higher dysfunction dysphasia, visuospatial disorder The Peer Teaching Society is not liable for false or misleading information Stroke (Bamford classification, cont.) Posterior circulation syndrome (POCS) one of:
Cerebellar / brainstem syndrome e.g. quadriplegia, locked in syndrome LoC Isolated homonymous hemianopia Cranial nerve palsy AND contralateral motor/sensory deficit Lacunar syndrome (subcortical stroke due to small vessel disease) one of: Pure motor stroke contralateral weakness of face, arm, leg, or all 3 Ataxic hemiparesis ipsilateral weakness + clumsiness (mostly affects legs) Pure sensory stroke contralateral numbness, tingling, pain, or burning Mixed sensorimotor stroke
Clumsy hand dysarthria The Peer Teaching Society is not liable for false or misleading information Stroke (investigations and management) Need to distinguish between hemorrhagic & ischaemic stroke CT brain Ischaemic 1st line thrombolysis 2nd line aspirin 300mg for 2 weeks then clopidogrel 75mg OD
Haemorrhagic Control BP: B-blocker Beriplex if warfarin-related bleed Clot evacuation Rehab Physio, OT, SALT Risk factor management Anti-hypertensives, statins
The Peer Teaching Society is not liable for false or misleading information TIA (presentation) TIA sudden onset global neurological deficit lasting <24h sudden onset global neurological deficit lasting <24h with complete clinical recovery (usually 5-15m) Features of carotid/anterior blockage (80%)? x3 Hemiparesis unilateral weakness (and/or hemisensory loss) Amaurosis fugax descending loss of vision in one eye (ipsilateral retinal/ophthalmic artery embolism) Brocas (expressive) dysphasia Features of vertebrobasilar/posterior blockage? (lots!)
Hemisensory symptoms Diplopia, vertigo, vomiting, dysarthria (leading to slurred speech), ataxia Hemianopia (ophthalmic cortex) or bilateral visual loss The Peer Teaching Society is not liable for false or misleading information TIA (assessment) ABCD2 score:
Age 60 1 point BP 140/90 1 point Clinical features: Unilateral weakness 2 points Speech disturbance without weakness 1 point Duration of symptoms: >60 mins 2 points 10-59 mins 1 point Diabetes 1 point
The Peer Teaching Society is not liable for false or misleading information TIA (management) If high risk of stroke (ABCD2 4 / >1 TIA/week / AF / on anticoagulant) following TIA: Antiplatelet aspirin 300mg (or clopidogrel 300mg) unless on anticoagulant therapy Statin simvastatin 40mg If on anticoagulant therapy admit for imaging to rule out haemorrhagic stroke Secondary prevention Lifestyle advice stop smoking, exercise, etc.
Control risk factors treat HTN, AF, DM Which drugs could you prescribe to help? x2 Clopidogrel 75mg Statin What could you offer patients who have 50-90% carotid stenosis? Carotid endarterectomy The Peer Teaching Society is not liable for false or misleading information Subarachnoid haemorrhage Aetiology 1. Usually result of bleeding from berry aneurysm at branching points in Circle of Willis
Origin of anterior communicating artery Joining of posterior communicating artery with ICA 2. Congenital AV malformations 3. Idiopathic Risk factors Smoking, alcohol, HTN, bleeding disorders, Marfan + ED syndromes, autosomal dominant PKD The Peer Teaching Society is not liable for false or misleading information SAH (presentation)
Sentinel headache (headache, dizziness, orbital pain) in 3 weeks prior to SAH due to small warning bleeds Symptoms: Sudden onset severe occipital sudden onset global neurological deficit lasting <24h thunderclap headache Others nausea + vomiting, neck stiffness, seizures, drowsiness Signs:
Meningism neck stiffness, Kernigs sign, photophobia Fundoscopy intraocular haemorrhages Signs of ICP Focal neurology e.g. pupil changes + other signs of 3rd nerve palsy if posterior communicating artery aneurysm The Peer Teaching Society is not liable for false or misleading information SAH (investigations and management) Investigations: 1. CT head white star-shape due to blood in basal cisterns 2. Lumbar puncture wait 12 hours LP result shows xanthochromia (yellowing) why? Breakdown of RBCs increased bilirubin
Management: Nimodipine decreases cerebral artery vasospasm so prevents cerebral ischaemia Surgery coiling (endovascular obliteration) preferred to clipping The Peer Teaching Society is not liable for false or misleading information Subdural and epidural haematoma Subdural haematoma Which people are affected? Elderly + alcoholics Why are they affected? x3
Brain atrophy Vein stretching Increased likelihood to fall The Peer Teaching Society is not liable for false or misleading information Subdural and extradural haematoma (cont.) Subdural Cause of bleeding? How does the level of consciousness differ? What are some features of ICP? x4
Extradural Fracture of temporal Rupture of bridging bone leading to tear of veins running from middle meningeal artery cortex to venous sinuses Fluctuating levels of consciousness but ICP gradually rises over some weeks
Headache Vomiting Confusion Seizures The Peer Teaching Society is not liable for false or misleading information Brief period of unconsciousness, then a lucid interval of improvement, then condition rapidly deteriorates as ICP increases
Subdural and extradural haematoma (cont.) Investigation CT head LP contraindicated why? Coning The Peer Teaching Society is not liable for false or misleading information Subdural and extradural haematoma (cont.) Management First thing that should be done? ABCDE Next how would you treat raised ICP? Osmotic diuresis with mannitol
Surgery SDH emergency evacuation via Burr hole craniotomy EDH clot evacuation +/- ligation of bleeding vessel The Peer Teaching Society is not liable for false or misleading information Epilepsy (presentation) sudden onset global neurological deficit lasting <24h Recurrent tendency to have spontaneous, intermittent and abnormal electrical activity in a part of the brain, manifesting as seizures Prodrome aura ictal symptoms post-ictal symptoms Prodrome = mood/behaviour change Aura = part of seizure patient is aware of Ictal symptoms = dependent on part of brain affected Post-ictal symptoms = headache, confusion, amnesia, etc.
The Peer Teaching Society is not liable for false or misleading information Epilepsy (classification) Partial (focal) seizures limited to 1 hemisphere Temporal (most common) Smell/taste abnormalities, auditory phenomena Automatisms lip smacking, walking without purpose Memory phenomena dj-vu/jamais-vu Frontal Motor phenomena (may lead to Jacksonian march (spreading clonic movement Jacksonian march) Occipital visual phenomena Parietal sensory disturbances tingling, numbness, etc.
The Peer Teaching Society is not liable for false or misleading information Epilepsy (classification) Generalised seizures simultaneous electrical discharge through cortex Absence transient LoC <10s, abrupt onset + termination Myoclonic sudden, brief jerking of limb/face/trunk Tonic increased tone Tonic-clonic 1. Tonic phase (LoC + increased tone of limbs) 2. Clonic phase (rhythmical jerking of limbs)
Atonic no LoC, sudden loss of muscle tone e.g. drop of hand or fall The Peer Teaching Society is not liable for false or misleading information Epilepsy (management) Partial (focal)? Tonic-clonic? Tonic, atonic? Absence?
Myoclonic? Carbamazepine, lamotrigine Sodium valproate Valproate Valproate / ethosuximide Valproate / levetiracetam Contraindicated in tonic, atonic, absence and myoclonic? Carbamazepine
The Peer Teaching Society is not liable for false or misleading information Epilepsy (management) Status epilepticus (seizure >5m) emergency Open + maintain airway, give O2 and gain IV access Community buccal midazolam or rectal diazepam Hospital IV lorazepam/diazepam Give phenytoin if seizures continue The Peer Teaching Society is not liable for false or misleading information Parkinsons Disease Pathophysiology Dopamine synthesis: L-tyrosine L-DOPA Dopamine Where is dopamine produced?
Substantia nigra apoptosis here leads to PD The Peer Teaching Society is not liable for false or misleading information PD (presentation) What are the textbook signs? x3 Bradykinesia slowness of movement Resting tremor starts unilaterally, improved by voluntary movement Rigidity (cog-wheel) increased tone and spasticity Other features? x3 Micrographia Postural changes stoop, shuffling + festinant (hurrying) gait Non-motor features decreased sense of smell, constipation, frequency/urgency
The Peer Teaching Society is not liable for false or misleading information PD (differentials) What are the differentials for PD? x4 Benign essential tremor Parkinson-plus syndromes VIVID o o o o o Vertical gaze palsy progressive supranuclear palsy Impotence/Incontinence multiple system atrophy Visual hallucinations Lewy body dementia Interfering activity by limb cortico-basal degeneration
Diabetic/hypertensive patient vascular parkinsonism Drugs antipsychotics, metoclopramide, prochlorperazine Rarer causes trauma (e.g. boxing), Wilsons disease, HIV The Peer Teaching Society is not liable for false or misleading information PD (management) What drugs could you use to increase dopamine supply? Co-careldopa: L-DOPA (levodopa) + carbidopa Dopamine receptor agonists ropinirole/rotigotine What types of drugs could you use to decrease dopamine breakdown? MAO-B inhibitor rasagiline/selegiline COMT inhibitor entacapone/tolcapone
Drugs that could help the tremor? Anticholinergic, amantadine The Peer Teaching Society is not liable for false or misleading information Huntingtons Disease Pathophysiology What type of genetic condition is this? Autosomal dominant What triplet of huntingtin gene is repeated and how many repeats are need for diagnosis? CAG, >39 repeats required
Atrophy of which part of the brain leads to the depletion of GABA? Striatum Less GABA less regulation of dopamine to striatum increased dopamine levels and increased movement The Peer Teaching Society is not liable for false or misleading information HD (presentation) What are the early features? Irritability, depression, self-neglect, behavioural problems, etc.
What are the main features of advanced disease? Chorea and rigidity (which progresses to dystonia) Dementia Some differentials? Sydenhams chorea, benign hereditary chorea, drug induced (e.g. LDOPA), other dyskinesias, other causes of dementia The Peer Teaching Society is not liable for false or misleading information Headaches Classification Primary tension, cluster, migraine Secondary meningitis, encephalitis, GCA, medication overuse, venous thrombosis, tumour, SAH Other trigeminal neuralgia
The Peer Teaching Society is not liable for false or misleading information Tension headache Classification Episodic TH <15d per month Chronic TH >15d per month, can be medication induced, also associated with depression Cause Neurovascular irritation which refers to scalp muscles and soft tissues The Peer Teaching Society is not liable for false or misleading information Tension headache (cont.) Presentation What type of pain and where is it felt?
Generalised mild-moderate pressing/tightening pain bilaterally Range of time it can last for? 30 minutes to 7 days Treatment (as well as reassurance, stress relief, etc.) Types of drugs used for simple cases and chronic cases? Simple ibuprofen, aspirin, etc. Chronic TCA e.g. amitriptyline The Peer Teaching Society is not liable for false or misleading information Cluster headache Presentation What type of onset where is the pain? Rapid onset severe unilateral, orbital, supraorbital or temporal pain
Range of time it can last for? 15-180 minutes What time of day do patients say they get these headaches? Middle of night or morning hours (occurs after REM sleep) Other symptoms? x4 Ipsilateral eye lacrimation & redness, rhinorrea, miosis and/or ptosis The Peer Teaching Society is not liable for false or misleading information Cluster headache (cont.) Treatment Acute case (name of drug, route administered)? Subcutaneous sumatriptan
What else? 100% oxygen through non-rebreathable mask for 15 minutes What drugs can be used as prevention? x3 Verapamil, lithium carbonate, prednisolone The Peer Teaching Society is not liable for false or misleading information Migraine Triggers CHOCOLATE:
Chocolate Hangovers Orgasms Cheese Oral contraceptive pill Lie-ins Alcohol Tumult Exercise The Peer Teaching Society is not liable for false or misleading information
Migraine (presentation) Migraine without aura 4 diagnostic criteria: 5 attacks Lasting 4-72h 2 of the following 4:
Unilateral Pulsating Moderate/severe pain Aggravation by (or avoidance of) routine physical activity 1 of the following: Nausea and/or vomiting Photophobia and phonophobia The Peer Teaching Society is not liable for false or misleading information
Migraine (presentation) Migraine with aura 2 diagnostic criteria: 1 reversible aura symptom Visual zigzags, spots Unilateral sensory tingling, numbness Speech aphasia Motor weakness (known as sudden onset global neurological deficit lasting <24h hemiplegic migraine so rule out stroke & TIA)
2 of the following 4: 1 aura symptom spreads gradually over 5m and/or 2 aura symptoms occurring in succession Each aura symptom lasts 5-60m 1 aura symptom is unilateral Aura accompanied/followed within 60m by headache The Peer Teaching Society is not liable for false or misleading information Migraine (management) Conservative avoid triggers, stop pill How would you treat an acute migraine (mild + severe)? Mild attack aspirin/ibuprofen +/- anti-emetic (e.g. metoclopramide) Severe attack sumatriptan + NSAID/paracetamol
What are the methods used for prophylaxis? x3 1. Propranolol or topiramate 2. Acupuncture 3. Amitriptyline / pizotifen The Peer Teaching Society is not liable for false or misleading information Giant cell arteritis How does it present? Tender, thickened, pulseless temporal arteries Jaw claudication pain on chewing
Scalp tenderness pain on combing hair Visual disturbance amaurosis fugax sudden onset global neurological deficit lasting <24h curtain falling over one eye (can be irreversible) Systemic features malaise, fever, lethargy, weight loss, polymyalgia rheumatic features The Peer Teaching Society is not liable for false or misleading information GCA (cont.) Investigations and treatment Bloods results?
What else needs to be done? ANCA Negative ESR >50 CRP Raised ALP
Raised Hb Lowered Temporal artery biopsy shows necrotising arteritis with inflammation What 2 drugs would you prescribe to treat this patient? High dose oral prednisolone (40mg) + low dose aspirin (75mg) Which other drugs need to be prescribed with the steroids?
PPI (gastric protection) & bisphosphonate (bone protection) The Peer Teaching Society is not liable for false or misleading information Trigeminal neuralgia 4 diagnostic criteria: 1. 3 attacks of unilateral facial pain 2. Pain in 1 division of trigeminal nerve with no radiation 3. Pain must have 3 of the following: Paroxysmal attacks lasting from 1-180 seconds
Severe intensity Electric shock-like/shooting/stabbing/sharp Precipitated by innocuous stimuli to the affected side of the face (vibration, washing/shaving, brushing teeth, etc.) 4. No neurological deficit The Peer Teaching Society is not liable for false or misleading information Trigeminal neuralgia (cont.) Treatment 1st line? Carbamazepine 100mg 2nd and 3rd line? Lamotrigine, phenytoin or gabapentin
Surgery rhizotomy (to deliberately damage nerve), stereotactic radiosurgery, etc. The Peer Teaching Society is not liable for false or misleading information Cauda Equina syndrome Bundle of spinal nerves from the level of L1/2 Horses tail Tumours, disc herniation, trauma can cause the compression Back pain Saddle anesthesia Do PR Loss of bowel / bladder control MRI
Treatment Surgical decompression Multiple Sclerosis Etiology Chronic autoimmune disorder of the CNS Plaques of demyelination Common sites are optic nerves, brainstem, cervical spinal cord Types Relapse and remitting Primary progressive Secondary progressive Multiple Sclerosis
Typical patient Young female 2 distinct clinical episodes of CNS dysfunction Remission in a few weeks Ix MRI brain and spine Evoked potentials LP shows oligoclonal IgG bands in CSF Multiple Sclerosis Management Acute Steroids = Methylprednisolone Chronic
1st line = Beta Interferon, Glatiramer acetate 2nd line = Natalizumab Symptom management Tremor = BB, Spasticity = Baclofen PT, OT, MDT Myasthenia Gravis Characterized by weakness and fatigability of ocular, bulbar and proximal limb muscles Ptosis, talking and chewing problems, swallowing IgG antibodies attach to AChR at the postsynaptic membrane at the NMJ Associated with a thymic tumour in 10%
Myasthenia Gravis Lots of drugs can aggravate Myasthenia Gravis BBs, Lithium, Some antibiotics Investigations Bedside tests Count to 50 / keep your arm outstretched Bloods Anti-AChR antibodies in blood Can also have Anti-MuSK antibodies Tensilon test (rarely performed) CT/MRI for thymoma Myasthenia Gravis
Treatment Anticholinesterases Pyridostigmine Immunosupressants Prednisolone, azathioprine Plasmapheresis IVIG used in myasthenic crisis Thymectomy Motor Neuron Disease UMN LMN
DISUSE ATROPHY Hypo-reflexia Hypo-tonia Denervation atrophy Babinski -ve Motor Neuron Disease Dysfunction of MOTOR NEURONES No sensory disturbances Destruction in the anterior horn cells of brain and spinal cord Four types Most patients have a mixed picture ALS is the most common
SOD-1 gene Motor Neuron Disease Clinical presentation Fasciculations are characteristic Can affect UMN and LMN so varied picture Investigations EMG Raised creatinine kinases due to muscle destruction Motor Neuron Disease Treatment Riluzole Na+ channel blocker works on Glutamate
Treat symptoms Tracheostomy, ventilator, NG tube PT/OT/MDT Death Usually due to respiratory failure because of pneumonia Guillain Barr-syndrome ACUTE neuropathy Inflammatory and demyelinating Triggered by infection Campylobacter Jejuni, EBV, CMV
Guillain Barr-syndrome Progressive onset of limb weakness after viral illness Loss of reflexes Often sensory and motor disturbances Vary from mild to severe Severe can cause respiratory depression Vital capacity should be monitored if suspected Guillain Barr-syndrome Investigations Mainly a clinical diagnosis Nerve conduction studies LP shows high protein in CSF Treatment
IVIG Ventilation is respiratory muscles involved Peripheral neuropathies Mononeuropathies = one nerve Median, Radial, Sciatic, Common Peroneal Polyneuropathies = multiple nerves DAVID Diabetes
Alcohol Vitamin deficiency (B12) Infective (GB) Drugs (isoniazid) Carpal Tunnel Syndrome Trapped median nerve Pregnancy, Obesity, Hypothyroidism, RA Tinnels and Phalens tests Pain relief -> Splint -> Steroid injection > Surgery Meningitis Inflammation of the meninges Neck stiffness, headache, photophobia
Can be viral or bacterial Viral is often self-limiting HSV, EBV, HIV, Mumps The Peer Teaching Society is not liable for false or misleading information Bacterial Meningitis Bacterial is medical emergency Neisseria meningitides Streptococcus pneumonia Listeria monocytogenes Inflammation of the meninges Neck stiffness, headache, photophobia
Fever , +ve kernigs sign, Non-blanching rash = meningococcal septicaemia The Peer Teaching Society is not liable for false or misleading information Bacterial Meningitis TREAT FIRST, INVESTIGATE LATER Treatment Benzylpenicillin in the community Cefotaxime in the hospital Contact tracing Investigations LP CSF analysis (protein, colour, glucose) Head CT
If other signs such as papilledema or seizures Bloods Subsequent treatment depends on investigations and culture Encephalitis Infection of the actual brain parenchyma Unlike meningitis, cerebral function is often altered Can still get meningeal signs and symptoms though Can be viral or bacterial Herpes Simplex Virus is dangerous Treat with high dose I.V acyclovir The Peer Teaching Society is not liable for false or misleading information
Herpes Zoster Initial infection of Herpes Zoster = chicken pox Reactivation = shingles Varicella lies dormant in the DRG RFs for reactivation Old age, poor immune system, chickenpox < 18 months age Dermatomal distribution of rash and pain Give oral acyclovir Other things to go over
Spinal tracts Syphillis Brain Tumours Neuro-anatomy Basal ganglia Exam Qs 2016 SAQ: Dense hemiparesis and aphasia (focus on psychosocial aspects) SBA: Inhibitory neurotransmitter GABA Neurotransmitters of ANS acetylcholine? Microorganism causing meningitis Nerves of the hand
Visual pathways Initiation and control of ongoing voluntary movements The Peer Teaching Society is not liable for false or misleading information Top Tips LECTURES LECTURES LECTURES PAST PAPERS PAST PAPERS PAST PAPERS
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