Neurological Conditions Flashcards

Question

What is epilepsy, criteria to be classified as epilepsy

Answer 1

Neurological condition characterised by recurrent seizures (excessive activity of cortical neurones resulting in transient neurological symptoms) Has to have more than 2 seziures more than 24 hours apart for diagnosis

Answer 2

Primary= idiopathic Secondary= tumour meningitis vasculitis alcohol withdrawal haemorrhage metabolic Conditions linked- cerebral palsy, tuberous sclerosis, mitochondrial disease

Answer 3

Focal- localised to specific cortical regions, can be complex (consciousness affected) or non-complex (consciousness not affected) Simple focal seizures: twitching or a change in sensation, such as a strange taste or smell. Complex focal seizures :confused or dazed, unable to respond to questions or direction for up to a few minutes. Generalised seizure- affects whole brain, consciousness lost immediately. 5 types - absence: rapid blinking or stare into space - tonic: Muscles in the body become stiff. - atonic: Muscles in the body relax. - tonic-clonic: stiff then jerking/spasm movements, may cry out and fall. -myoclonic: Periods of shaking or jerking parts on the body. Status epilepticus a seizure lasting longer than 5 mins, or 2 or more seizures within a 5 minute period without the person retuning to normal inbetween. Have to rule out hypoxia and hypoglycaemia thru blood gluose

Answer 4

FOCAL SEIZURE - frontal: motor convulsions, post-ictal flaccid weakness, jacksonian march (clonic movements starting in one extremity then spreads e.g. in little finger twitching/tingling up arm) - frontal lobe complex- loss of consiousness, involuntary actions, rapid recovery - Temporal lobe seizure features? Aura- involving: Weird smell, iInvoluntary movements, Deja vu, Abdo pain Lip smacking/plucking/grabbing (automatisms) Post-ictal dysphasia Hallucinations - Occipital lobe seizure Visual disturbances (flashers and floaters) - Parietal lobe seizure Sensory issues (paraesthesia- tingling, numbness) GENERALISED SEIZURES - Tonic-clonic seizure Vague symptoms before attack e.g. irritability Tonic phase (generalised muscle spasm- goes stiff and falls to floor) Clonic phase (repetitive synchronous jerks- jerking limbs or loss of bladder control) Urinary incontinence Tongue biting Post-ictal phase - Impaired consciousness - Lethargy - Confusion - Absence seizure Onset in childhood Loss of consciousness but maintained posture (don’t fall down) No post-ictal phase Often begins abruptly without warning and ends abruptly Patient has no recollection of episode Stares blankly into space EEG shows 3 Hz spike and wave - Myoclonic seizure convulsions without the muscle tensing (tonic phase) Sudden jerking of limb, trunk or face with preserved consciousness - Atonic seizure sudden muscle relaxation causing patients to fall to the ground and then may motionless incontinence post-ictal confusion - Tonic seizure muscle tensing without convulsions (clonic phase)

Answer 5

Clinical diagnosis- 2 or more 24 hours apart EEG- confirm diagnosis and classify MRI- check for structural, space occupying or vascular lesions that may cause midline shift. Bloods- capillary blood glucose (exclude hypoglycaemia), electrolytes (hypocalcaemia and hyponatraemia), prolactin (seizure vs psudoseizure)

Answer 6

only start treatment after more than 2 unprovoked seizures FOCAL 1st- lamotrigine or levetiracetam 2nd- carbamazepine GENERALISED SEIZURES (NOT ABSENCE) - Men: sodium valporate -Women: lamotrigine (levetiracetam if myoclonic) ABSENCE 1st: Ethosuximide Men 2nd- sodium valporate Women 2nd- lamotragine/levetiracetam STATUS EPILEPTICUS Hospital- IV lorezapem Community- PR diazepam If doesnt work another dose of IV lorezapem, if that doesnt work then IV phenytoin MAX 2 DOSES OF BENZODIAZEPINES DVLA 1st unprovoked seizure= 6 months off driving abnormal brain image or eeg= 12 months off driving

Answer 7

COMP: fractured from tonic-clonic behavioural problems sudden death complications to anti-epileptic drugs -Lamotrigine= can cause steven johnson syndrome, large blistering rash over body -Carbamazipine= SIADH, drowsiness, steven johnsons syndrome, neutropenia, osteoporosis -sodium valporate: weight gain -phenytoin= gingival hypertrophy, peripheral neuropathy Prognosis- 50% remission at 1 year

Answer 8

Progressive, mainly symmetrical, rhythmic, involuntary oscillation movement disorder of the hands and forearms. Absent at rest, present during posture and intentional movements Bimodal distribution- teens and elderly Family history - as its autosomal dominant inheritance

Answer 9

Bilateral upper limb action tremor- absence of other neurological signs Worse with sustained voluntary movement like outstretched arms, stress or anxiety 90% hands, head 30%, voice 15% may have intention or resting tremor improves with alochol consumption

Answer 10

clinical diagnosis alone

Answer 11

if no dysfunction/mild- just observation If dysfunction- 1st line propranolol or primidone. 2nd line gabapentin. If both drugs have no effect then Deep Brain Stimulation

Answer 12

Comp- DBS complications like hameorrhage or infection Prog- persistant and preogressive condition, many mild cases dont seek treatment

Answer 13

Parasitic infection caused by the protozoa of the genus plasmodium- plasmodium falciparum is most life threatening is a NOTIFIABLE DISEASE Tropical and subtropical regions- travellers account for most cases in western countries Bite by an infected female anopheles mosquito OR blood tranfusion OR organ transplantation RF- travel to an endemic area (african countries), inedequate chemoprophylaxis, not using insecticide-treated bed net in endemic areas Protective factors - sickle cell anaemia, G6PD deficiency

Answer 14

Cyclical fevers with chills and rigors (shivering)- aka sever cold/rigors followed by severe sweating, alternates days Haemolytic anaemia- causes jaundice and may turn urine dark Splenomegaly Headache Weakness Myalgia Arthralgia Anorexia Diarrhoea

Answer 15

Giemsa stained thick and thin blood smears- detects asexual or sexual forms of the parasites inside erythrocytes Thick- detects parasites present Thin- detects species FBC- check for anaemia Rapid Diagnostic Tests- detect parasite antigen or enzyme

Answer 16

Chloroquine (ok if preg) or Hydroxychloroquine Primiquine once symptoms resolve to presvent relapse Prevention- avoid exposure use nets, repellant, protective clothing and prophylaxis

Answer 17

Comp: AKI- dehydration and hypovolaemia Hypoglycaemia Metabolic acidosis Severe anemia Seizures ARDS Prog- sever if low host immunity, pregnant, younger than 5, immunocompromised, older adults

Answer 18

Infection of the meninges in the brain or spinal cord, commonly viral or bacterial- may be fungal parasitic or due to noninfectious cause Less than 1 years old or 43 years old RF- immunocompromised, crowded living conditions, otitis media, sinusitis, CSF leak after head trauma or neurosurgery, sepsis

Answer 19

BACTERIAL (serious) - Neonates: Group B streptococcus (extended labour, infection in previous pregnancy). Listeria monocytogenes - Children- Streptococcus pneumoniae (Gram+ diplococci)(PNEUMONIA = POSITIVE) or neisseria meningitidis (Gram - diplococci, causes non-blanching rash) (NEISSERIA NEGATIVE NON BLANCHING) -Elderly- sterptococcus pneumoniae (gram +). Listeria monocytogenes VIRAL (common) - Enteroviruses (poliovirus, coxsakie) : most common cause HSV VZV mumps

Answer 20

bacterial + viral similar but VIRAL is LESS ACUTE and usually self limiting within 7-10 days Triad- fever, headache, neck stiffness Photophobia Nausea and Vomiting Altered mental state seizures Deafness Meningococcal meningitis= non blanching rash Kernig sign- cant straighten leg when hip flexed to 90 Brudzinski sign- forced flexion of neck result in reflex flexion of hips Neonates: lethargy, irritability, poor appetite, vomiting, fontanelle bulging, seizures

Answer 21

CT head first (before lumbar puncture) if increased ICP is suspected as LP can cause sudden decrease in pressure and lead to brain herniation Lumbar puncture- CSF analysis (only is no signs of riased ICP - vomiting, blurred vision, headache, less alert) - BACTERIAL: ""cloudy"", ""high neutrophils"" (granular), high protein, ""LOW glucose"", normal openig pressure - VIRAL: ""clear"", ""high lymphocytes"", normal/high protein, normal glucose, normal opening pressure - TB: ""slightly cloudy/fibrin web"", ""high lymphocytes"", high protein, ""LOW glucose"", ""high opening pressure"" Blood Cultures: obtain 2 sets before antibiotic therapy

Answer 22

Primary care- as soon as suspected IV or IM Benzylpenicillin or IV/IM cefotaxime or ceftriaxone and send to hospital If LP contraindicated (sepsis/evolving rash sign, severe resp/cardiac compromise, signifiant bleeding risk, raised ICP sign ( papulloedema, neurological sign, seizure, GCS 12 or less) then: -Bloods - Immediate IV ABs : cefotaxime or ceftriaxone (if theyre over 50yrs old then add amoxicillin) - IV Dexamethosone shortly before or with first dose of ABs (reduces complication risk) - If ICP raised: secure airway + high flow oxygen, bloods and blood cultures from IV, IV dexamethosone, IV ABs, Do CT scan) If LP isnt contraindicated -Bloods and blood culures -LP without CT - Immediate IV ABs : cefotaxime or ceftriaxone (if theyre over 50yrs old then add amoxicillin) - IV Dexamethosone shortly before or with first dose of ABs (reduces complication risk) AVOID in meningococcal septicaemia - Viral- supportive measures as usually self limiting (maybe antiviral) Close contacts: -Prophylactic ABs to close contacts of meningococcal meningitis - oral ciprofloxacin or rifampicin SUSPECTED Bacterial meningitis Over 3 moths- IV ceftriaxone. Dexamethasone Lower than 3 months- IV cefotsxime plus amoxicillin (can give caftriaxone IF no jaundice, not premature, normal albumin, no acidosis, no calcium containing infusions) If travelled abroad- vancomycin WHEN CALCIUM- cefotaxime not ceftriaxone CONFIRMED BACTERIAL Younger than 3 months: Group B- IV cefotaxime Listeria Monocytogenes- IV amoxicillin and gentamicin (gentamicin for first 7 days only) Gram negative bacilli: cefotaxime Older than 3 months: H influenza - IV cefatriaxone Pneumoniae (same) UNCONFIRMED BACTERIAL MENINGITIS younger than 3 months- cefotaxime plus amoxicillin Over 3 months- ceftriaxone MENINGOCOCCAL IV ceftriaxone 7 days If only suspected then do the same

Answer 23

Comp- deafness, spticaemia, shock, disseminated intravascular coagnulation, cerebral oedema, renal failure, cranial nerve lesion Prognosis- Bacterial is fatal untreated Viral resolves spontaneously mostly

Answer 24

Chronic, episodic neurological disorder that has a strong genetic component and usually presents in early to mid life. Primary headache characterised by recurrent episodes of unilateral localised pain F:M 3:1 Adolescence and early childhood Three types: -migraine with aura (classic migraine) - migraine without aura (common migraine) -migraine variant (familial hemiplegic, opthalmoplegic) Risk Factors: FHx migraine, female, menstruation, stress, obesity, sleep disorders, medication overuse, Triggers (CHOCOLATE) Chocolate Hangovers Orgasms Cheese/Caffiene Oral Contraceptive Lie ins Alcohol Travel Exercise

Answer 25

Prolonged unilateral headache- 4-72hours, recurrent episodes Throbbing/pulsatile pain Nausea Aura before- flashing lights Photophobia and Phonophobia- quiet dark room needed Headache worse with activity Decreased ability to function (affects daily activity) Abdominal pain associated in children

Answer 26

Migraine: Unilateral, 4-72 hr, pulsing throbbing pain with nausea, photophobia or phonophobia. may have aura T- NSAIDs, tripatan. Prophylaxis- lifestyle change, B blockers, topiramate Tension: Bilateral, over 30 min, band like pain, no photophobia or phonophobia or aura T- analgestic, NSAID, acetaminophen Prophylaxis- TCA (amitryptaline) Cluster: Unilateral, 15min-3hr, periorbital pain with lacrimation and rhinorrhea. Horner syndrome maybe T- sumatriptan, 100% O2 therapy Prophylaxis- verapamil

Answer 27

Clinical diagnosis by history and physical exam Can do: ESR (raised in temporal arteritis) Lumbar puncture (SAH or meningitis) MRI or CT brain

Answer 28

ALL PT : Limit stimuli (light and noise) and activity. Nausea with IV fluids and anti-emetics (metoclopramide) 1st line - oral triptan (sumatriptan)+ NSAID - dont use triptan with coronary artery disease patients as can cause coronary vasospasm - 12-17 year olds can have nasal triptans rather than oral Prophylaxis (more than 2 per month)= propanolol or topiramate - Propanolol avoided in asthmatics bcs bronchoconstriction - Propanolol preferred in pregnant women and women of child bearing age as topiramate can cause cleft lip Medicine for headaches can trigger medication overuse headaches if so then: -Stop all medication including: simple analgesia: paracetomol, NSAIDs + triptans - If was on opioid then withdraw gradually Pregnant pt: 1st Paracetomol 2nd NSAIDs in first and second trimester Avoid aspirin and opioids in pregnancy Individuals that have migraine with aura should not have combined pill

Answer 29

Inc risk of pre-eclampsia Inc risk of depression Analgesia overuse headaches Prog- most do well

Answer 30

Intense sharp stabbing pain around one eye 1-2 times per day 15min to 2 hours restless and agitated during attack as severe Clusters last 4-12 weeks redness, lacrimation, lid swelling Nasal stuffiness Miosis and ptosis - horners syndrome

Answer 31

MRI with gadolinium contrast

Answer 32

Subcut triptan and 100% O2 therapy Triptan not to be used if have coronary artery diseasr Prophylaxis: verapamil

Answer 33

Neurodegenerative disease with upper and lower motor neurone dysfunction Males, over 65 FHx of ALS in 5-10% of cases Cause unknown Types: 1) Ayotrophic lateral sclerosis- UMN and LMN signs 2) Progressive muscular atrophy- only LMN signs, best prognosis 3) Primary lateral sclerosis- UMN signs only 4) Prograssive bulbar palsy variant- tongue and bulbar involvement (dysarthria, dysphagia) - worst prognosis Those with MND at risk of developing frontotemporal dementia

Answer 34

Progressive muscle weakness Fasciculations Dysphagia- bulbar onset ALS may present with difficulty swallowing Shortness of breath Eye movements spared, normal sensation Wasting of thenar muscles and wasting of tongue base UMN sign- spasticity, hyper-reflexia, clonus, positive babinski sign, brisk limb and jaw reflex, dysarthria, dysphagia, loss of dexterity LMN sign- hypotonia, hyporelexia, muscle atrophy, tongue fasciculations and fibrillations , dysphagia, weakness, nasal speech Assymetrical symptoms

Answer 35

Clinical diagnosis assess history and examination Electromyography EMG- show denervation Normal nerve conuction studies to rule out neuropathy MRI- exclude cord compression Spirometry to monitor respiratory muscle weakness

Answer 36

1st line- Riluzole a glutamate agonist, prolongs life by 3 months Repiratory care- BIPAP (NIV) at night for type 2 resp failure Percutaneus gastronomy (PEG) tube if difficulty swallowing and poor nutrition

Answer 37

COMP: Respiratory failure Nutritional deficit Aspiration pneumonia Fronto-temporal dementia Prog: die within 3-5 years

Answer 38

Chronic degenerative disease of the CNS caused by immune-mediated inflammatory processes. Results in demyelination and axonal degeneration in the brain and spinal cord. Dissemination in time and space- lesions in the CNS must have occurred in at least 2 different places and at least 2 different times. Female3:Male1, 20-40 years old, white people (young white female) Three forms: 1) Relapsing-remitting - Acute attacks last 1-2 month with complete recovery inbetween 2) Secondary progressive disease- A relapsing remitting patient who has deteriorated and developed neurological signs and symptoms between relapses 3) Primary progressive MS- Progressive deterioration from onset, no remission/relapse period Cause: genetic prediscposition, environmental risk factors ( low vitamin D, smoking, EBV)

Answer 39

Optic neuritis: first manifestation, unilateral impaired vision, colour blindness, pain in moving eye, RAPD (both pupils illuminated in swinging flashlight test Intrauclear opthalmoplegia- lesion of the medial longitudinal fasciculus blocking connection between contralateral 6th nerve nucleus and ipsilateral 3rd nerve nucleus affecting horizontal gaze - Ipsilateral impaired adduction (temporal) e.g. right MLF lesion so right eye cant look at nose - Nystagmus in eye abducting (moving nasally) e.g right MLG lesion so left eye can still abduct (look temporally) by is shaky Headache and fatigue Sensory disturbances (patchy paraesthesia) Weak after walking UMN signs- positive babinski, spasticity, hyperreflexia Leg cramping Bladder disorders (urinary incontinence) Lhermittes sign- paraesthesia in limbs on neck felxion Hoffmans sign- flicking/putting pressure on nail bed causes twitching of thumb of thumb or fingers Unthoffs phenomenon- neurological symptoms are exacerbated by inc in body temp e.g. after hot baths or exercise

Answer 40

MRI Brain with contrast- view demyelinating lesions, more white/translucency around the ventricles MRI Spinal cord with contrast : see white blob in middle of spinal cord Lumbar Puncture + CSF Examination - oligoclonal bands+ elevated levels og IgG antibodies Visually Evoked Potentials- optic neuritis leads to demyelination of optic nerve so slower conduction times = prolonged visually evoked potential

Answer 41

For relapse as steroids dont help when return to baseline just shorten relapse: 1st- IV glucocorticoids (methylprednisolone) 2nd- plasma exchange Reduce risk ofelpasing: Immunomodulators (beta-interferon) or natalizumab Spasticity: baclofen or gabapentin

Answer 42

COMP: UTI Osteopenia+ Osteoporosis Depression Visual Impairment Erectile Dysfunction Cognitive Impairment Impaired Mobility Prognosis: hgih relapse rate in first 2 years after onset

Answer 43

Autoimmune neuromuscular disease characterised by generalised muscle weakness Cause: Autoantibodies against post-synaptic nicotinic Ach receptors (AChR) at the neuromuscular junction F>M Associated with thymomas (tumour of anterior mediastinum and thymic hyperplasia. Thymomas can cause SVC obstruction RF- other autoimmune conditions

Answer 44

Muscle fatiguability- worse with activity, improves on rest (so worse at end of day) Ptosis and diplopia Dysphagia - difficult swallowing Dysarthria - changes in speech Facial Paresis Proximal Limb weakness Respiratory Muscle weakness- lead to dyspnoea

Answer 45

Serum AChR antibody analysis- positive is specific for myasthenia gravis Electromyography (EMG)- shows decremental response to repetitive nerve stimulation. most Sensitive test CT thorax-look for thymoma Muscle specific Tyrosine Kinase antibodies- positive Tensilonn test- IV edrophonium reduces muscle weakness temporarily. Not used much bcs cardiac arrythmia risk

Answer 46

Beta blockers can make worse, can cause FVC to drop due to muscle weakness

Answer 47

1st- Long acting acetylcholinesterase inhibitors (pyridostigmine). If take too much then cholinergic crisis (too much ACh= cramps, increased salivation, lacrimation, muscular weakness, paralysis, muscular fasciculation, diarrhea, and blurry vision) Corticosteroids (prednisolone) if symptoms dont resolve Acute myasthnic crisis = plasma exchange/plasmapheresis and IV immunoglobulins Surgery- thymectomy : minimise need for immunosuppressants AVOID BETA BLOCKERS

Answer 48

COMP: Myasthenic crisis ( give plasmapheresis and IV immunoglobulins), respiratorny failure, impaired swallowing, acute aspiration, secondary pneumonia Prognosis- most have good QoL

Answer 49

Degeneration of dopaminergic neurones in the basal ganglia, particularly the substantia nigra M2:F1, over 65 yrs RF- genetic, enviromental factors (MPTP exposure- a drug that damages substantia nigra), drug-induced (anti-psychotics)

Answer 50

Parkinson’s Disease A progressive brain disorder with movement and non-movement symptoms Symptoms worsen slowly over time Movement symptoms tend to improve with levodopa Parkinsonism= Signs include slowness (bradykinesia), stiffness (rigidity) and resting tremor. parkinsonism symptoms progress quicker and often do not respond as well to levodopa. Atypical Parkinsonism A group of progressive brain disorders with some of the symptoms seen in PD Symptoms are often more serious early on and progress quicker Movement symptoms improve less or not at all with levodopa 1) Lewy Body dementia: -memory loss -visual hallucinations -2) Progressive supranuclear palsy - Postural instability/falls - Impaired vertical gaze (hard to read or go down stairs) - Cognitive impairment 3) Multisystem atrophy - Postural hypotension- bp high when lay down -Incontinence -Impotence/ erectile dysfuncyion 4) Corticobasal syndrome -jerky, involuntary movements -loss of function on one side Secondary Parkinsonism Conditions that can look like PD, but are not always progressive Symptoms may improve by treating the underlying cause Movement symptoms usually do not improve with levodopa - Drug induced parkinsonism (antipsychotics like haloperidol and anti sickness like metoclopramide) p- procyclidine for tremor - brain tumours - normal pressure hydrocephalus

Answer 51

1st - Urgent referral to neurology, medication can only be given by specialists Durgs given aim to increase dopamine in substantia nigra If motor symptoms affect quality of life 1st- levodopa or co-careldopa - can have on-off effect - nausea is side effect so give domperidone - SE- dystonia, chorea and athetosis (involuntary writhing If motor symptoms do not affect quality of life: -Levodopa -Dopamine agonists (ropinerole, pramipexole, apomorphine)SE= impulse disorders likepathological gambling -MAO-B inhibitors (rasagiline) or COMT inhibitors (entacapone) - All CRITICAL medicines and should not be stopped even on acute admission to hospital- need to be continuous to stop syptoms reoccuring Vit D supplements Physical therapy: -Exercise -Occupational therapy -Speech therapy AVOID ANTIPSYCHOTICS

Answer 52

COMP- dementia, constipation, depression, anxiety PROG- progressive no cure

Answer 53

Bradykinesia - slowness of movement, shuffling gait, slow turning Resting tremor- asymmetrical onset, improves with voluntary movement, pill-rolling, 3-5Hz Rigidity- lead pipe (smooth risistance to passive movement of limb e.g elbow fexion) and cogwheel (jerky rigidity when passively flexing arm) Postural Insability- imbalance or falling, festination (involuntary quickening), shuffling gait TRAP- tremor, rigidity, achalasia, prostural instability Other symptoms: fatigue, constipation, depression, anxiety, insomia, hypomimia (reduced facial expression)

Answer 54

Diagnosis= clinical history and presenting features Dopaminergic Agent Trial (DAT scan)- should improve symptoms Single Proton Emission Computed Tomography (SPECT)

Answer 55

excess cerebrospinal fluid accumulates in the brain’s ventricles, but normal pressure

Answer 56

wet, wacky, wobbly Urinary incontinence Dementia Gait abnormality similar to parkinsons Neuroimaging- Ventriculomegaly without sulcal enlargement / or out of proportion to sulcal englargement

Answer 57

Result from systemic diseases (like diabetes and autoimmune disease) or localised damaged (trauma, compression, tumours) and manifest with neurological deficits distal to the level of the lesion Cause Injury - accidents can cut crush or compress nerves Medical Conditions- diabetes, guillian-barre syndrome , carpal tunnel syndrome Autoimmune Disease- SLE, RA, sjorens syndrome

Answer 58

Neuropraxia → compression injury causing temporary disruption of nerve conduction Axonotmesis → axon is damaged but the perineurium and epineurium remain intact Neurotmesis→ complete nerve transection Traumatic Neuroma→ benign, painful nodular thickening caused by nerve regeneration at the site of different forms of nerve injury

Answer 59

immune mediated demyelination of peripheral nervous system usually a few weeks after injection (e.g campylobacter jejuni) get back/leg pain, progressive symmetrical weakness of all limbs starts in legs then reaches arms, absent reflexes LP- rise in protein but normal WCC Conduction velocity- decreased as demyelination

Answer 60

Compression of median nerve in carpal tunnel Cause- pregnancy, oedema, RA Symptoms- pins and needles in thumb, index and middle finger. weakness of thumb adduction, wasting of thenar eminance, Tinels sign (tapping causes parasthesia), Phalens sign (flexion of wrist causes symptoms) Nerve conduction studies EMG Steroid injections, wrist splints at night If severe- surgical decompression

Answer 61

Motor nerves: mucle weakness, painful cramps, uncontrollable muscle twitching Sensory nerves: paraesthesia in hands and feet, trouble sensing pain or change in temp, walking Autonomic nerves: excessive sweating, changes in bp, cant tolerate heat, GI symptoms

Answer 62

MEDIAN NERVE INJURY - Wasting of thenar eminence - Loss of sensation in lateral palmar surface of 3 and a half digits - Weakness in abductor pollicis brevis Median nerve usually effected by Carpal tunnel syndrome Median nerve= C6-T1 ULNAR NERVE INJURIES - Wasting of hypothenar eminence - Loss of sensation over medial 1 and a half digits - Weakness in abductor digiti minimi - Claw hand Ulnar nerve= C8-T1 RADIAL NERVE INJURIES - Weakness of wrist extension → wrist drop - Anaesthesia over first dorsal interosseous muscle Radial nerve= C5-T1 KLUMPKE'S PALSY - Paralysis of intrinsic muscles of hand - Loss of sensation in ulnar distribution - Horner’s syndrome sometimes present Spinal cord level C8-T1 ERB'S PALSY - Loss of shoulder abduction and elbow flexion - Arm held internally rotated - Waiter’s tip Spinal cord level C5-C6 PEREONEAL NERVE INJURY - Weakness in dorsiflexion and eversion of foot → foot drop - Sensory loss over dorsum of foot - Hit in side of knee Spinal Cord Level L4-S1 L5 Radiculopathy would present with weakness of hip abduction and loss of inversion of foot TIBIAL NERVE INJURY - Inability to invert foot or stand on tiptoe - Sensory loss on sole of foot Spinal Cord Level L4-S3

Answer 63

Foot Drop ⇒ may be due to common peroneal nerve lesion (most common) or L5 radiculopathy. Common peroneal nerve lesion occurs due to compression at neck of fibula. Weakness of foot dorsiflexion and eversion. Weakness of hip abduction suggests L5 radiculopathy.

Answer 64

Plain X-ray or CT/MRI EMG or Nerve Conduction Studies

Answer 65

1st line- conservative unless open injury - Expectant management (allowing spontaneous recovery with close monitoring) - Activity modification - Splinting - Electrical stimulation - Physiotherapy - Analgesia Nerve repair or nerve transfer (if injury not healing properly on its own or if open injury)

Answer 66

MAIN SYMPTOMS - Pain starting in area where spinal nerve roots are dysfunctional and radiates down to dermatome (shooting pain) - Motor- LMN symptoms for muscles innervated by this spinal root e.g. hyporeflexia - Biceps ⇒ C5, C6 - Triceps ⇒ C7, C8 (Radial Nerve) - Knee ⇒ L3, L4 - Ankle ⇒ S1, S2 C5, C6 pick up the sticks. C7, C8 lay them straight. L3, L4 kick the door. S1, S2 buckle my shoe. - Sensory- dermatomal pattern of pain and numbness

Answer 67

Pinched nerve ROOT- condition where one or more nerves are affected and do not work properly Happens when surrounding bone or tissue (cartilarge, muscles or tendons) put pressure on the nerve and disrupt its function (neuropathy is issue with nerves, radiculopathy is issue with nerve roots) CAUSE: mechanical compression of nerve root, intervertebral disk herniation, degenerative disc disease, osteoarthritis

Answer 68

CERVICAL RADICULOPATHY Neck pain, headache, shoulder pain C3/4 radiculopathy affects C2-C4 disks, shoulder and neck areas sensory deficits, scapular winging motor deficit C5 radiculopathy affects C4-5 disks, affects sensation in anterior shoulder, affects bicep and deltoid movement, bicep reflex affected C6 Radiculopathy affectc C5-6 disks, affects lateral side of elbow to thumb and lateral part of index finger, affects bicep and wrist extensors C7 Radiculopathy affects C6-C7 disks, sensory deficity in middle finger and half of fingers 2 and 4, dorsal medial forearm. Affects movement of triceps, wrist flexors and finger extensors C8 Radiculopathy affects C7-T1 disk. Sensation loss in half of 4th finger and pinky finger, hypothenar eminence and ulnar aspect of the distal forearm. Motor affects finger flexors, no reflex affected

Answer 69

Most common radiculopathy Sciatica : compression of the sciatic nerve (lumbrosacral roots L4,L5,S1) Cause: herniated intravertebral disk Clinical Features: pain and tingling radiating from lower back to ipsilateral leg, weakness in calf muscles Investigations: Straiht le raise test (pain on passive flexion of leg = lasegue's sign) Treatment: Physiotherapy, NSAIDs, if no improvement in 4-6 weeks then MRI

Answer 70

Lower back pain and leg pain, standing/sitting makes both worse. bending forward makes better as straightens the spine a bit L5 specific symptoms = foot drop (weakness/paralysis of dorsiflexion and eversion of the foot), weakness of hip abduction and inversion of the foot, sesnosy loss over L5 dermatome, lower back pain that shoots down leg Cause: Lumbosacral disk herniation, common pereoneal nerve lesion (compression at neck of fibula) L3 radiculopathy affects L2-L3 disk, sensation impaired in anterior thigh (L2) medial thigh and over the knee (L3). Motor deficits in hip flexion, knee extension and hip adduction. Adductor reflex and patellar reflex affected L4 radiculopathy affects L3-L4 disks. Sensory deficit in medial thight, area over patella(L3), medial aspect of leg , medial malleous(L4). Motor deficits in knee extension and hip adduction. Patellar reflex affected L5 radiculopathy affects L4-5 disks. Sensory deficits in lateral aspect of thigh and knee, anterolateral aspect of the leg, dorsum of the foor and the big toe. Motor deficits in dorsiflexion of foot difficult heel walking as foot drop. big toe cant dorsiflex Posterior tibial reflex S1 radiculopathy affects L5-S1 disks. Sensory deficit in the dorsolateral aspect of the thigh and leg and the lateral aspect of the foot. Motor cant evert foot and cant plantar flex foot (cant toe walk). Achilles reflex and latral hamstring impaired S2/3/4 radiculopathy affects S1-4. Sensory deficit of posterior aspect of thigh and leg S2, perineum S3-4 and perianal S4. No motor issues. Bulbocavernous refex and perineal reflex affected

Answer 71

Positive straight leg raise test EMG to assess nerve function MRI spine if doesnt improve with conservative treatment

Answer 72

`conservative- NSAIDs, steroid injection, physiotherapy. if symptoms dont improve in 4-6 weeks then MRI Surgery if significant neurological defects

Answer 73

Lumbosacral nerve root compression at L4/5 or L5/S1. Central disk prolapse Lower back pain, bilateral sciatica, reduced perianal sensation, decreased anal tone, urinary dysfunction, Urgernt MRI and surgical decompression

Answer 74

Brain and ventricles encased by skull so cant accomodate additional volume, if volume increases it leads to raised ICP Causes: -Idiopathic Intracranial hypertension: young overweight females -CNS infection= meningitis -Space occupying lesions= haemorrhage, tumours) -Increased CSF= hydrocephalus -cerebral oedema -increased BP (malignany hypertension Normal ICP= 15mmHg or less for adults in supine position

Answer 75

Cushing Triad- irregular breathing, widening pulse pressure, bradycardia = triad reflects brainstem compression Bilateral Headache- worse in morning and after lying down. Worse when coughing/straining Vomiting Reduced consciousness Bilateral visual loss (optic nerve compression-visual field testing) Sixth nerve palsy Papilloedema- (swelling of optic disk-see on fundoscopy)

Answer 76

CT Head (no contrast)/ MRI HEad Intraventricular catheter (invasive)= motitoring put into ventricles with a CSF draining system, useful when CSF drainage is required for diagnostic and therapeutic reasons. ICP of over 20 indicates this is needed

Answer 77

If young, overweight female, Ct shows enlarged arachnoid outpouchings and prominent perivascular spaces and could be taking a tetracycline like doxycyline= weight loss and acetazolamide. 1st- Head elevation to 30 degrees IV Mannitol (osmotic diuretic- hyperosmolar solution helping to draw water out the brain to reduce pressure CSF Drainage if too much CSF through: intraventricular catheter (hydrocephalus) repeated lumbar puncture (e.g. idiopathic intracranial hypertension) ventriculoperitoneal shunt (for hydrocephalus) Controlled Hyperventialtion- reduced pCO2 which causes vasoconstriction of cerebral arteries= reduced ICP Glucocorticoids- Dexamethosone, do if raised ICP is due to infection or inflammation like meningitis Emergency Surgery- resection of tumour, haematoma evacuation

Answer 78

Cerebral oedema Decreased cerebral perfusion pressure Brain tissue herniation

Answer 79

An injury to the spinal cord resulting from processes that compress or displace arterial, venous, and cerebrospinal fluid spaces, as well as the cord itself Causes: Infection Trauma- usually acute onset Vertebral compression fractures (low energy trauma in pts with osteoporosis or osteomyelitis)- usually chronic onset Vertebral metastasis (most common): from lung, breast, prostate, usually chronic onset Intervertebral disk disease (herniation)- usually acute onset 16-30 yaers old- trauma most common 30-50 disk herniation 40-75+- malignancy

Answer 80

Lumbosacral nerve roots (L3-5) that extend below spinal cord are compressed Cause Disc herniation (L4/L5 or L5/S1) - Decreased reflexes - Saddle anaesthesia - Faecal incontinence - Urinary incontinence - Bilateral sciatica - Decreased anal tone Treat = Urgent MRI and then possible surgical decompression

Answer 81

Back pain → earliest and most common symptom, if its worse when lying down or coughing its a red flag for tumours or growths Paraesthesia or numbness/sensory loss at level of lesion (LMN) Weakness or paralysis bilaterally below affected level of spinal cord (UMN) Bladder or bowel dysfunction- faecal incontinence and urinary retention Hyperreflexia See UMN signs below the level of the lesion and LMN signs at the level of the lesion

Answer 82

MRI Spine (whole spine)- look for disk displacement or mass, recommended within 24 hours of presentation

Answer 83

Depends on cause 1) Trauma spinal cord compression: - Immobilisation - Decompressive surgery - IV corticosteroids (e.g. dexamethasone) 2) intervertebral disc compression (including cauda equina) Decompressive laminectomy 3) Malignancy High dose oral dexamethosone

Answer 84

COMP: Pressure ulcers, UTI, DVT Prog- depends on cause

Answer 85

An acute neurological condition resulting from a disruption in cerebral perfusion, lasting more than 24 hours - Ischaemic stroke (85%) cerebral infarction due to insufficient blood flow due to a thrombus or embolus - Haemorrhagic stroke (15%) cerebral infarction due to haemorrhage (rupture of blood vessel causing leakage of blood into the brain) RF: - Age >65 - Hypertension - Diabetes - AF - Obesity - Smoking - High cholesterol

Answer 86

BAMFORD STROKE CLASSIFICATION TACS (total anterior circulation stroke) vs PACS (partial anterior circulation stroke) TACS is 3/3, PACD is 2/3 1) Unilateral weakness and/or sensory deficit of the face arm and leg 2)Homonymous hemianopia 3) Higher cerebral dysfunction (dysphagia, visuospatial disorder) LACS (lacunar syndrome) one of the following -pure sensory stroke -pure motor stroke -sensory-motor stroke -ataxic hemiparesis POCS (Posterior circulation syndrome) one of following: -cranial nerve palsy and a contralateral motor/sensory deficit - bilateral motor/sensory deficit -conjugate eye movement disorder like gaze palsy - cerebellar dysfunction- ataxia, nystagmus, vertigo -isolated homonymous hemianopia or cortical blindness

Answer 87

All acute onset MIDDLE CEREBRAL ARTERY 1) Contralateral weakness and sensory loss in upper limbs and lower half of face 2) Contralateral homonymous hemianopia 3) Aphasia: - Broca's area (left frontal lobe) causes Expressive aphasia → it’s responsible for speech production - Wernicke's area (left temporal lobe) causes Receptive aphasia → it’s responsible for speech comprehension ANTERIOR CEREBRAL ARTERY 1) Contralateral weakness and sensory loss in lower limbs 2) Abulia (behaviour changes) 3) Urinary incontinence POSTERIOR CEREBRAL ARTERY 1) Contralateral homonymous hemianopia with macular sparing 2) Visual agnosia (difficulty recognising familiar objects/faces) 3) Contralateral sensory loss 4) Memory deficits 5) Vertigo 6) Nausea 7) Stroke of midbrain branches of the posterior artery cause ipsilateral oculomotor palsy (down and out eye) and contralateral weakness of the upper and lower extremity POSTERIOR CIRCULATION STROKE 1) Damage to the brainstem 2) Ipsilateral symptoms 3) Cerebellar signs (DANISH) - Dysdiadochokinesia - Ataxia - Nystagmus - Intention tremor - Slurred speech - Hypotonia POSTERIOR INFERIOR CEREBELLAR ARTERY STROKE Lateral medullary syndrome: - cerebellar signs - Nystagmus - Vertigo and vomiting - ipsilateral facial pain and temp loss - contralateral upper and lower limb pain and temp loss - ipsilateral Horner's ANTERIOR INFERIOR CEREBELLAR ARTERY STROKE - Sudden onset vertigo and vomiting - ipsilateral facial paralysis - deafness WEBER'S SYNDROME A form of midbrain stroke characterised by: - ipsilateral CN III palsy - contralateral hemiparesis PONTINE HAEMORRHAGE - reduced GCS - paralysis - bilateral pin point pupils BASILAR ARTERY STROKE Locked in syndrome → decreased GCS and motor symptoms POSTERIOR COMMUNICATING ARTERY ANNEURYSM - 3rd nerve palsy (down and out eye, dilated pupil) - Eye pain

Answer 88

Wernicke’s aphasia symptoms - Speech fluent - Comprehension abnormal - Repetition impaired Broca’s aphasia symptoms - Speech non-fluent, laboured, and halting - Comprehension normal - Repetition impaired Conduction aphasia symptom - Speech fluent - Comprehension normal - Repetition impaired. Aware of the errors they are making Global aphasia symptoms - Speech non-fluent - Comprehension impaired - Repetition impaired Speech non fluent ? Comprehension intact= brocas Comprhension not intact= global Speech fluent? Comprehension intact= conduction aphasia Comprehension not intact= wernickes

Answer 89

ROSIER (Recognition of stroke in the emergency room) helps define between stroke and stroke mimics Non-contrast CT-head: to exclude haemorrhage and confirm ischaemic stroke CT angiogram: Look for which vessel is occluded After patient been treated look for cause of stroke - ECG to look for structural heard diseases - Ambulatory ECG to look for atrial fibrillation - Carotid doppler (if more than 70% occluded then do carotid endarteretomy to remove plaque) Assess disability after a stroke using : Barthel index

Answer 90

1st- CT head before thrombolysis to rule out haemorrhage (esp if on warfarin/DOAC/has bleeding disorder) - less than 4.5hours since onset= do thrombolysis (IV alteplase) - for ACA within 6 hours do thrombectomy and thrombolysis (or for Posterior circulation over 24 hours) (thrombolysis contraindicated if previous intercranial haemorrhage, seizure with onset of stroke, suspec subarachnoid haemorrhage, had stoke or traumatic brain injurt in last 3 month, pregnanct, actively bleeding, GI bleed in last 3 weeks, oesophageal varices, lumbar puncture in past week, intercranial neoplasm, uncontrolled hypertension above 200/120, INR over 1.7, hameorrhagic diathesis, active diabetic hameorrhagic retinopathy, major surgey in last 2 weeks, suspected intracardiac thrombus - if more than 4.5 hours conservative management - 300mg oral aspirin with swallow assessment - after two weeks stop 300mg aspirin, start 75mg clopidogrel for life. If cant take clopidogrel then Apirin and modified release dipyridamole - if stroke was due to atrial fibrillation then : anticoagulation DOAC initiated 2 weeks after stroke IF ipsilateral carotid artery stenosis over 70% then do carotid endarterectomy - risk of hypoglossal nerve being damaged IF hameorrhagic stroke patient Stop anticoagulants (if on warfarin consider vitamin K and prothrombin concentrate,, also control BP if acute) FOR TIA once haemorrhage rules out start anticoagulation immediately If ischaemic stroke then start anticoagulation after 2 weeks

Answer 91

If think TIA: specialist and do MRI if TIA or Stroke that have symptomatic carotid stenosis 50-99% NASCET or 70-99% ECST - Referral urgently for carotid endarterectomy - Blood pressure, anti platelet, cholesterol, lifestyle, diet TIA or stroke pts who have symptomatic carotid artery stenosis less than 50% NASCE or less than 70 ECST - Do not have surgery - Blood pressure, anti platelet, cholesterol control, lifestyle SUSPECT ACUTE STROKE Non enhanced CT IMMEDIATELY IF - Indication for thrombolysis or thrombectomy - On anticoagulant - Known bleeding issue - GCS under 13 - Progressive or fluctuating symptoms - Papilloedema, neck stiffness or fever - Severe headache on onset of symptoms If thrombectomy indicated: imaging with CT contrast angiography after this non enhanced CT If thrombectomy indicated but after 6 hours: CT perfusion imaging ACUTE ISCHAEMIC STROKE THROMBOLYSIS (ATLEPLASE) IF: - Within 4.5h since symptom onset - Between 4.5-9h since symptom onset AND imaging shows potential to salvage tissue - If woken with symptoms: Within 9h of midpoint of sleep AND potential to salvage tissue (Assuming no contraindications, and haemorrhagic stroke excluded). MECHANICAL THROMBECTOMY IF: - Within 6h of symptom onset, with occlusion of proximal anterior circulation - Between 6-24h of symptom onset/wellness, with occlusion of proximal anterior circulation AND potential to salvage brain tissue - Within 24h of symptom onset/wellness, with occlusion of proximal posterior circulation (i.e. basilar / posterior cerebral atery) AND potential to salvage brain tissue (Assuming adequate pre-stroke functional status). If a person meets criteria for thrombolysis and mechanical thrombectomy, both can be given. MOST IMPORTANT: Within 4.5h, exclude haemorrhage, then give thrombolysis. Within 6h, if proximal anterior circulation stroke, do mechanical thrombectomy. (Add thrombolysis regardless if also meets under 4.5h criteria) Beyond this, you need to do a CT perfusion / diffusion-weighted MRI scan to assess the potential to salvage brain tissue. ASPIRIN AND ANTICOAGULATION Aspirin 300mg orally or if have dysphagia then rectall. Continue for 2 weeks If have AF or a clotting disorder don’t start aspirin until imaging confirmed Prosthetic valve stop their treatment for a week and do aspirin conservative management - 300mg oral aspirin with swallow assessment - after two weeks stop 300mg aspirin, start 75mg clopidogrel for life. If cant take clopidogrel then Apirin and modified release dipyridamole - if stroke was due to atrial fibrillation then : anticoagulation DOAC initiated 2 weeks after stroke instead of clopidogrel

Answer 92

Bleeding into the subarachnoid space (between arachnoid and pia) and is an emergency Causes - Traumatic SAH- head trauma - Non-traumatic SAH = ruptured intracranial aneurysm (in circle of Willis then called berry aneurysm), arteriovenous malformations, anticoagulant use RF: - Age ≥50 y/o - Smoking - Alcohol - Hypertension - Family history of polycystic kidney disease (autosomal dominant) - FH

Answer 93

- Thunderclap Headache → severe, sudden-onset, occipital headache within 1-5 mins and lasts >1 hour - Reduced level of consciousness - Meningeal signs - neck stiffness - photophobia - N&V - seizures - muscle aches

Answer 94

1st line - Non-contrast CT Head- diagnostic see hyperdense area in subarachnoid space → particularly in outline of circle of Willis and vasculature If CT head is done less than 6 hours after symptom onset and is normal - dont lumbar puncture, may be something else If CT is done after 6 hours and its normal - do lumbar puncture, Lp should be done 12 hours after onset to allow development of xanthochromia - biliirubin in CSF as RBC breaking down- the CSF sample will be yellow If SAH is confirmed do CT angiogram to confirm location of bleed in vessel and the cause Can do ECG to check for: -arrhythmia -prolonged QT (torsades de pointes) - ST segment or T wave abnormalities Electrolytes- Hyponatremia often found due to SIADH

Answer 95

Stop anticoagulants immediately Nimodipine (calcium channel blocker) to prevent vasospasm as it can narrow blood vessel and block leading to ischaemia Platinum endovascular coiling to treat intracranial aneurysms (clip it to stop bleeding)

Answer 96

COMP- re-bleeding vasospasm - delayed cerebral ischaemia hyponatreamia SIADH seizure hydrocephalus PROG- overall outcome is poor

Answer 97

Collection of blood between the dural and arachnoid coverings of the brain. Usually due to rupturing of bridging veins between the cortex and venous sinus. As the volume of the hameorrhage increases the brain parenchyma is compressed and displaced and the ICP may rise and cause herniation TYPES 1) Acute: less thna 3 days old, hyperdense bleed on imaging, normally trauma 2) Subacute: 4-20 days old with hyperdense bleed on imaging 3) Chronic: more than 20 days old, hypOdense bleed on imaging, usually from rupture of veins RF - Recent trauma - Coagulopathy or anticoagulant use - Alcohol use - Advanced age >65 years old Common demographic: Males over 65

Answer 98

- Can present several weeks after initial head injury - Gradual continuous headache → sign of raised ICP - Nausea/vomiting - Fluctuating confusion/consciousness or loss of consciousness - Diminished eye, verbal and motor response (low GCS) - Seizures - Lucid interval Several weeks to month progressive history of either confusion, reduced consciousness or neurological deficit

Answer 99

Non contrast CT scan- See a cresent shaped bleed not limited by suture lines. If acute/subacute then hyperdense (white) bleed as its fresh blood, if chronic then hypodense as older (might be black cresent shaped). May cause a midline shift to contralateral side, crosses cranial sutures (aka not onfined by skull sutures) but does not cross midline If CT inconclusive then MRI

Answer 100

Small- non complicated bleed: -stop anticoagulants/antiplatelets -start prophylactic antiepileptics (phenytoin or levetiracetam -observe Large bleed (over 10mm) Acute → decompressive craniotomy Chronic → burr hole evacuation Chronic Bleed -stop anticoagulants/antiplatelts -start antiepileptics (phenytoin or levetiracetam) Monitor ICP and try to reduce

Answer 101

COMP -neurological deficity -coma -epilepsy Prognosis →Acute SDH has a higher likelihood of an underlying parenchymal injury and is therefore associated with a worse prognosis than acute EDH. The prognosis of chronic SDH is better than that of acute SDH, however chronic SDH is associated with higher mortality with increasing age.

Answer 102

Primary headache disorder → most common type of headache overall Exacerbating factors - Fatigue - Lack of sleep - Poor posture - Anxiety - Stress - Depression - Missing meals Female 20-39 years old

Answer 103

- Episodic nature, lasts 30 mins to a couple of days - Band-like headache, often bilateral - May radiate to neck/shoulders - Dull, pressing, non-pulsating in character (lower intensity than migraines) - Relieved with painkillers - Headache doesn’t increase with exertion - No nausea, vomiting or aura (unlike migraines)

Answer 104

Usually clinical diagnosis

Answer 105

1st line : Aspirin, paracetomol, NSAIDs prophylactic- amytriptyline or acupuncture Lifestyle change - Exercise - Weight reduction - Reduce mental tension

Answer 106

COMP peptic ulcers (due to NSAID use) Prog- self treatment with analgesia usually effective

Answer 107

Temporary, focal cerebral ischaemia that results in reversible neurological deficits without acute infarction that resolves completely with 24 hrs Men and incidence increases with age - AF- most common - Valvular disease - Carotid stenosis - Congestive heart failure - Hypertension - DM - Smoking

Answer 108

- Sudden onset & brief duration of symptoms (most patients have resolution within 1 hour) - Unilateral weakness or paralysis - Dysphasia- indicates left sided ischaemia - Ataxia, vertigo or loss of balance- indicates posterior TIA - Homonymous hemianopia - Diplopia

Answer 109

Urgent Carotid Doppler CT head- if patient has bleeding disorder or is on anticoagulants to rule our haemorrhage MRI brain with diffusion weighted imagine - to determine location ECG- look for AF and rule out myocardial ischaemia Bloods -Blood glucose: exclude hypoglycaemia as the cause - PT, INR, APTT: to exclude coagulopathy ABCD2 score- estimate stroke risk

Answer 110

GOLD STANDARD Antiplatelet therapy - 300mg or clopidogrel for 2 weeks, after that 75mg clopidogrel for life If already on anticoagulants do CT head to rule out haemorrhage Treat BP only if only 220/120 If present within 7 days of episode= specialist review within 24 hours If present after 7 days= specialist review within 7 days Secondary long term prevention= Atorvastatin 80mg + antihypertensives Carotid endarterectomy → carotid artery stenosis >70% If atrial fibrillation give DOAC or Low Molecular Weight Heparin anticogulants Cannot drive for 1 month

Answer 111

COMP stroke myocardial infarction Prognosis → no residual symptoms from the primary event. However, patients have increased risk of future ischaemic stroe

Answer 112

A facial pain syndrome in the distribution of ≥1 divisions of the trigeminal nerve (Ophthalmic, Maxillary & Mandibular divisions). Caused by compression of the trigeminal nerve Females, 60-70 years old RF increased age multiple sclerosis Associated with HSV

Answer 113

Unilateral facial pain- severe sudden shooting stabbing (like electric shock) followed by burning ache. Lasts several seconds and may occur up to 100 times a day. Usually shoots from mouth to angle of jaw on affected side. Triggered by movements like chewing, talking or touch Red Flag symptoms (refer to specialist) - Sensory changes - Deafness or other ear problems - History of skin or oral lesions that could spread perineurally - Pain only in the ophthalmic division of the trigeminal nerve (eye socket, forehead, and nose), or bilaterally - Optic neuritis - A family history of multiple sclerosis - Age of onset before 40 years

Answer 114

Clinical diagnosis

Answer 115

Newly- Diagnosed- anticonvulsants (carbamazepine: this drug can cause SIADH and steven johnsons syndrome) If dont respond to medical therapy refer to neurology to get microvascular decompression

Answer 116

Acute, reversible condition caused by severe thiamine (vitamin B1) deficiency Causes - Chronic heavy alcohol use- most common - Inadequate intake or malabsorption of thiamine - Bariatric surgery predispose to thiamine malabsorption M>F due to increased frequency of alcoholism in men

Answer 117

Confusion Eye sign: - opthalmoplegia -nystagmus, diplopia, ptosis Gait ataxia- wide based takes small steps Mental slowing, impaired concentration and apathy COAT - Confusion - Oculomotor dysfunction (nystagmus + ophthalmoplegia) - Ataxia - Thiamine IV administration

Answer 118

Korsakoff Syndrome (Wernicke’s is acute and reversible) CART: - Confabulation (making things up) - Anterograde amnesia (cant create new memories) - Retrograde amnesia (cant recall past) - Temper altered

Answer 119

Clinical diagnosis usually Bloods: decreased thiamine MRI - showing atrophy of mamillary bodies Screening tools for alcohol withdrawal= CIWA Clinical Institute Withdrawal Assessment for Alcohol

Answer 120

1st- immediate IV thiamine (pabrinex) if patient just at risk and hasnt developed the condition then can supplement diet with thiamine If delirium tremens and hallucinations- add a benzodiazepine like chlordiazepoxide Abstinence from alcohol

Answer 121

COMP: ataxia Korsakoffs psychosis hearing loss seizure Prognosis- permanent brain injury if not treated early

Answer 122

Homonymous hemianopia (loose both fields of same side, lesion is controlateral to which visual field lost) - incongruous defects: lesion of optic tract - congruous defects: lesion of optic radiation or occipital cortex - macula sparing: lesion of occipital cortex Homonymous quadrantanopias - superior quadrantopia: lesion of the inferior optic radiations in the temporal lobe (Meyer's loop) - inferior quadrantopia: lesion of the superior optic radiations in the parietal lobe - mnemonic = PITS (Parietal-Inferior, Temporal-Superior) - Inferior and superior here refer to the quadrantanopia itself Bitemporal hemianopia - lesion of optic chiasm - upper quadrant defect > lower quadrant defect = inferior chiasmal compression, commonly a pituitary tumour - lower quadrant defect > upper quadrant defect = superior chiasmal compression, commonly a craniopharyngioma