Neurology Flashcards

Question

How do you treat migraines?

Answer 1

``` Reduce triggers Acute - Triptans eg sumatriptan - NSAIDs - +/- anti-emetic ```

Answer 2

Selectively stimulate 5-hydroxytryptamine receptors in brain Contraindicated in IHD, coronary spasm and uncontrolled high BP S/E arrhythmias or angina +/- MI

Answer 3

Less likely to get medication over-use headache | Avoid paracetamol or ibuprofen

Answer 4

If more than 2 attacks a month, or acute treatment required more than 2x a week Beta-blocker Tricyclic anti-depressant Anti-convulsant

Answer 5

Most chronic daily and recurrent headaches are tension headaches

Answer 6

Commonest primary headache Can be episodic < 15 days/month or chronic > 15 days/month for at least 3 months No organic cause

Answer 7

``` Stress Sleep deprivation Bad posture Hunger Eyestrain Anxiety Noise ```

Answer 8

Usually one of following - Bilateral, pressing/tight non-pulsatile, mild/moderate intensity, +/- scalp tenderness Without vomiting or sensitivity to head movement, no aura Not aggravated by physical acitivty Tight band-like sensation Pressure behind eyes, mild-moderate pain Headaches can last from 30 mins to 7 days Not attributed to another disorder

Answer 9

Migraine Cluster headache Giant cell arteritis Drug-induced headache

Answer 10

Clinical diagnosis from history

Answer 11

Reassurance and lifestyle advice - regular exercise, avoid triggers Stress relief Symptomatic treatment of episodes occuring > 2 days a week - Aspirin, paracetamol, NSAIDs, no opioids Limit analgesia to no more than 6 days a month to reduce chance of medication over use headaches Tricyclic antidepressants

Answer 12

Worsens whilst on regular analgesia especially opioids Other causes mixed analgesics eg co-codamol, ergotamine, triptans Common reason for episodic headache becoming chronic daily headache

Answer 13

Brief episode of neurological dysfunction due to temporary focal cerebral ischaemia without infarction Symptoms generally resolve within 24 hours

Answer 14

15% first strokes preceded by TIA, also foreshadowing of MI More common in men Black ethnicity at greater risk due to hypertension and atherosclerosis predisposition

Answer 15

Small vessel occlusion Atherothromboembolism from carotid chief cause Cardioembolism resulting from microemboli from - Mural thrombus post-MI or in AF - Valve disease - Prosthetic valve Hyperviscosity - Polycythaemia, sickle cell anaemia, extremely raised WCC or myeloma - Can result from hypoperfusion - most important to consider in young people - cardiac dysrhythmia, postural hypotension, decreased flow through atheromatous arteries

Answer 16

``` Increasing age Hypertension Smoking Diabetes Heart disease - valvular, ischaemic, or AF Past TIA Raised packed cell volume Peripheral arterial disease Polycythaemia vera Combined OC Hyperlipidaemia Excess alcohol Clotting disorder Vasculitis eg SLE, giant cell arteritis, rare risk factor ```

Answer 17

Cerebral ischaemia resulting in lack of O2 and nutrients to brain result in cerebral dysfunction Short lived period of ischaemia with symptoms only lasting a maximum of 5-15 minutes after onset and then resolves before irreversible cell death occurs Symptoms gradually progressing suggest different pathology eg demyelination, tumour or migraine

Answer 18

Sudden loss of function, usually only lasts for minutes Complete recovery and no evidence of infarction on imaging Site of TIA often suggested by symptoms

Answer 19

90% Weak, numb contralateral leg +/- similar if milder arm Hemiparesis - weakness of entire side of body Hemisensory disturbance Dysphasia Amaurosis fugaux- sudden transient loss of vision in one eye, temporary reduction in retinal, ophthalmic or ciliary blood flow leading to temporary retinal hypoxia, TIA causing this often first clinical evidence of ICA stenosis

Answer 20

``` 10% Diplopia Vertigo Chocking and dysarthria Ataxia Hemisensory loss Hemianopia vision loss Transient global amnesia Tetraparesis ```

Answer 21

Cannot differentiate from stroke until full recovery Hypoglycaemia, migraine aura, focal epilepsy Intracranial lesion - tumour or subdural haematoma Syncope due to arrhythmia Todd' paralysis - transient weakness of arm, hand or leg after seizure Retinal or vitreous haemorrhage Giant cell arteritis

Answer 22

``` Often solely on Hx Bloods - FBC - polycythaemia? - ESR - raised in vasculitis - Glucose - hypoglycaemia? - Creatinine, electrolytes - Cholesterol Carotid artery doppler USS to look for stenosis/atheroma MR/CT angiography if stenosis to determine extent ECG - AF/MI ischaemia CT/diffusion weight MRI Echo/cardiac monitoring to assess for cardiac cause ```

Answer 23

``` To assess risk of stroke after TIA - Age > 60 = 1 - BP > 140/90mmHg > 1 - Clinical features - Unilateral weakness = 2 - Speech disturbance w/o weakness = 1 - Duration of symptoms - Lasting more than 1 hour = 2 - Lasting 10-59 minutes = 1 - Diabetes = 1 Score greater than 6 strongly predicts stroke and referred to specialise immediately Score greater than 4 assessed by specialist with 24 hours All patients with suspected TIA seen within 7 days ```

Answer 24

AF More than 1 TIA in one week TIA whilst on anti-coagulant

Answer 25

Antiplatelet drugs - Aspirin immediatley + dipyridamole for 2 weeks then lower dose - P2Y12 inhibitor long term eg clopidogrel Anticoagulant in AF, mitral stenosis or recent big septal MI eg warfarin Long term statins Control CVS risk factors - antihypertensives, improve diet, stop smoking Don't drive for at least 4 weeks following TIA

Answer 26

Syndrome of rapid onset neurological deficit caused by focal, cerebral, spinal or retinal infarction Characterised by rapidly developing signs of focal or global disturbance of cerebral functions, lasting for more than 24 hours or leading to death

Answer 27

Major neurological disease of our time 3rd most common cause of death in high income countries - 11% all deaths in UK Leading cause of adult disability worldwide Higher rates in Asian and black African populations than Caucasian Uncommon under 40 Incidence increases with age More common in men Incidence falling due to more vigorous approach to risk factors in primary care ie statin use and control of BP Ischaemia/infarction 80% Haemorrhagic 17% Other causes 3%

Answer 28

Small vessel occlusion/thrombosis in situ Cardiac emboli from AF, MI or IE Large artery stenosis Atherothromboembolism Hypoperfusion, vasculitis, hyperviscosity Hypoperfusion - watershed stroke where sudden BP drop by more than 40mmHg, then low cerebral blood flow leading to global ischaemia and watershed infarcts in vulnerable areas of cortex between boundaries of different arterial territories

Answer 29

CNS bleeds due to trauma, aneurysm rupture, anti-coagulation, thrombolysis, carotid artery dissection, SAH

Answer 30

Vasculitis Thrombophilia SAH Carotid artery dissection - spontaneous/neck trauma Venous sinus thrombosis - very rare, may occur in pregnancy, hypercoagulable states and thrombotic disorders or with dehydration or malignancy - Leads to cortical infarction, seizures, raised ICP

Answer 31

``` Male Black/Asian Hypertension Past TIA Smoking DM Increasing age Heart disease (valvular/ischaemic) Alcohol Polycythaemia, thrombophilia AF Hypercholesterolaemia Combined OC Vasculitis IE ```

Answer 32

Arterial disease and atherosclerosis Thrombosis occurs at site of atheromatous plaque in carotid/vertebral/cerebral arteries Large artery stenosis acts as embolism source rather than occluding vessel hypertension results in small infarcts known as lacunes and/or gradual accumulation of diffuse ischaemic change in deep white matter

Answer 33

Hypertension resulting in micro-aneurysm rupture Cerebral amyloid angiopathy - deposition of amyloid B in walls of small and medium sized arteries in normotensive patients Space occupying lesions Young adults 1/5 strokes due to carotid/vertebral artery dissection

Answer 34

Leg weakness and sensory disturbance Gait apraxia - difficulty walking Truncal ataxia Incontinence Drowsiness - consciousness controlled partly by frontal lobe Akinetic mutism - decrease in spontaneous speech, stuporous state

Answer 35

Contralateral arm and leg weakness and sensory loss Hemianopia Aphasia and dysphasia (if in dominant hemisphere) Facial droop

Answer 36

Contralateral homonymous hemianopia Cortical blindness Visual agnosia - cannot interpret visual info Prosopagnosia - cannot detect faces Colour naming and discriminate problems Unilateral headache - rare in ischaemic stroke

Answer 37

More catastrophic as wide region supplied Likely to get locked in Motor deficits such as hemiparesis or tetraparesis and facial paralysis Dysarthria and speech impairment Vertigo, nausea and vomiting Visual disturbances Altered consciousness

Answer 38

Small cortical stroke in midbrain, internal capsule presenting with one of - Unilateral weakness and/or sensory deficit of face and arm, arm and leg or all three - Pure sensory loss - Ataxic hemiparesis (cerebellar or motor symptoms)

Answer 39

No reliable way of distinguishing between them Intracerebral haemorrhage associated with severe headache/coma (signs of raised ICP) Patients on oral anticoagulants assumed to have haemorrhagic unless proved otherwise

Answer 40

Hypoglycaemia Migraine aura Focal epilepsy Syncope due to arrhythmia

Answer 41

Urgent CT head/MRI before treatment - Rules out haemorrhagic stroke before beginning thrombolysis - Infarction seen as low density lesion - subtle changes evident within 3 hours - In MRI, hyper-intense within hours of onset Pulse, BP, ECG - Look for AF - Careful treating BP as may compromise cerebral perfusion Bloods - FBC - looking for thrombocytopenia and polycythaemia - Blood glucose - ruling out hypoglycaemia

Answer 42

Maximise reversible ischaemic tissue - Ensure dehydration - Keep O2 sats > 95% - If ischaemia stroke confirmed by CT then thrombolysis Thrombolysis - Can be give up to 4.5 hours post symptom onset - Rule out haemorrhage first - Tissue plasminogen activator IV alteplase - Start antiplatelet therapy clopidogrel 24 hours after thrombolysis If time of onset unknown then aspirin daily for 2 weeks then lifelong clopidogrel Haemorrhagic - Frequent GCS monitoring - Antiplatelets CI - Any anti-coagulants reversed for warfarin reversal used beriplex and vit K - Control hypertension - Manual decompression of raised ICP/diuretics - Surgery may be required

Answer 43

``` Recent surgery in last 3 months Recent arterial puncture Hx of active malignancy Evidence of brain aneurysm Patient on anti-coagulation Severe liver disease Acute pancreatitis Clotting disorder ```

Answer 44

Platelet treatment (lifelong) eg aspirin + dipyridamole/clopidogrel Cholesterol treatment like statins AF treatment - warfarin or NOACs eg pixiban BP treatment

Answer 45

Spontaneous bleeding into subarachnoid space - between arachnoid layer of meninges and pia mater Can often be catastrophic

Answer 46

Typical age 35-65 Account for 5% of strokes Most common cause is rupture of Berry aneurysms

Answer 47

``` Rupture of berry aneurysms (80%) - Rupture of junction of posterior communicating artery with internal carotid or anterior communicating artery with anterior cerebral artery (in circle of Willis) - 15% multiple - Associated with PKD, and coarctation of aorta Arteriovenous malformation (10%) - Vascular developmental malformation often with fistula between arterial and venous systems causing high flow through AVM and high-pressure arterialisation of draining veins No cause found (15%) Rare - Bleeding disorder - Mycotic aneurysms - endocarditis - Acute bacterial meningitis - Tumours ```

Answer 48

``` Hypertension Known aneurysm FHx Disease that predisposes you to aneurysm - PKD - Ehlers Danlos syndrome (hyper-mobile joints with increased skin elasticity) - Coarctation of aorta Smoking, bleeding disorders, post-menopausal decreased oestrogen ```

Answer 49

Most common cause ruptured aneurysm which leads to tissue ischaemia (less blood can reach tissue) as well as rapid raised ICP as blood, acts like space-occupying lesion, puts pressure on brain, resulting in deficits if not resolved quickly

Answer 50

Sudden onset severe occipital headache - thunder clap Depressed level of consciouness Coma/drowsiness may last for days Neck stiffness Kernig's sign (unable to extend patient's leg at knee when thigh flexed) Brudzinski's sign Retinal and vitreous bleeds Papilloedema Vision loss or diplopia Focal neurology at presentation (fixed dilated pupils - signs of CN3 palsy) Marked increase in BP as a reflex to following haemorrhage Sentinel headache - May earlier have experienced a sentinel headache due to small warning leak - Ask about Hx

Answer 51

``` Must be differentiated from migraine 50-60% no cause of headache Meningitis Intracerebral bleeds Cortical vein thrombosis ```

Answer 52

ABG - to exclude hypoxia Head CT - gold standard - Detects > 90% of SAH within 1st 48 hours - Seen as star shaped lesion due to blood filling in gyro patterns around brain and ventricles CT angiography if aneurysm confirmed to see extent Lumbar puncture - If CT normal but SAH still suspected - CSF uniformly bloody early on and becomes yellow after several hours due to Hb breakdown (xanthochromia) - Xanthochromia confirms SAH

Answer 53

Refer all proved SAH to neurosurgeon immediatrly Maintaun cerebral perfusion keeping well hydrated (IV fluids) and aim for BP < 160mmHg CCBs to reduce vasospasm and consequent morbidity from ischaemia IV/oral nimodipine Endovascular coiling - Preferred to surgical clipping since lower complication rate where possible - Promotes thrombosis and ablation of aneurysm - First line treatment where angiography shows aneurysm Surgery - intracranial stents and balloon remodelling for wide-necked aneurysms

Answer 54

Rebleeding Cerebral ischaemia due to vasospasm - can result in permanent deficit Hydrocephalus due to blockage of arachnoid granulations - requires ventricular or lumber drain Hyponatraemia

Answer 55

Caused by accumulation of blood in subdural space - between arachnoid and dura mater following rupture of bridging vein between cortex and venous sinus (vulnerable to deceleration injury) Considered very treatable in all those whose conscious level fluctuates and also in those having evolving stroke - especially if on anticoagulants

Answer 56

Most common where patient has small brain eg alcoholic or dementia or babies that have suffered trauma, or elderly with brain atrophy making bridging veins more vulnerable Majority from trauma but trauma often forgotten as so minor or so long ago Chronic, apparently spontaneous SDH common in elderly and also occurs with anticoagulants

Answer 57

Trauma either due to deceleration due to violent injury or due to dural metastases resulting in bleeding from bridging veins between cortex and venous sinus Bridging veins bleed and form haematoma between dura and arachnoid reducing pressure and bleeding stops Days/weeks later haematoma starts to autolyse due to massive increase in oncotic and osmotic pressure thus water sucked into haematoma resulting in haematoma enlargement Results in gradual rise in intra-cranial pressure over many weeks Shifting midline strucutres away from side of clot and if untreated leads to eventual tectorial herniation and coning

Answer 58

Traumatic head injury Cerebral atrophy/increasing age Alcoholism, anticoagulation and physical abuse of infant

Answer 59

Interval between injury and symptoms can be days to weeks or months Fluctuating level of consciousness +/- insidious physical or intellectual slowing Sleepiness Headache Personality change Unsteadiness Signs of ICP eg headache, vomiting, nausea, seizure and raised BP Focal neurology eg hemiparesis or sensory loss (occurs later) Seizures Stupor, coma, coning In elderly symptoms will develop slowly as brain has more compliance to raised ICP

Answer 60

Stroke, dementia, CNS masses eg tumours/abscesses SAH Extradural haemorrhage

Answer 61

CT head - Diffuse spreading, hyperdense crescent shaped hemisphere - As clot ages and protein degradation occurs becomes isodense and eventually hypodense - Shifting of midline structures MRI head for subacute and smaller haematomas

Answer 62

Assess and manage ABCs, prioritise head CT Stabilise patient Refer to neurosurgeons - irrigation/evacuation via burr twist drill and burr hole craniotomy Address cause of trauma IV mannitol to reduce ICP

Answer 63

Suspect this after head injury and conscious level falls or is slow to improve or there is a lucid interval Collection of blood between dura mater and bone usually caused by head injury

Answer 64

Most commonly due to traumatic head injury resulting in fracture of temporal or parietal bone causing laceration of middle meningeal artery - typically after trauma to temple

Answer 65

Usually occurs in young adults (rare < 2 and > 60)

Answer 66

Characteristic history - head injury, brief post-traumatic loss of consciousness or initial drowsiness, lucid interval Severe headache, nausea, vomiting, confusion, seizures due to rising ICP +/- hemiparesis with brisk reflexes Rapid rise in ICP as epidural space full of blood Ipsilateral pupil dilates, coma deepens, bilateral limb weakness develops and breathing becomes deep and irregular (brainstem compression) Decreased GCS and coning Death due to respiratory arrest Bradycardia and raised BP late signs

Answer 67

Epilepsy, carotid dissection, CO poisoning Subdural haematoma SAH Meningitis

Answer 68

CT head - gold standard - Shows hyperdense haematoma that is biconvex and adjacent to skull - Blood forms more rounded shape compared with sickle shaped subdural haematoma Skull x-ray - may be normal or show fracture lines crossing course of middle meningeal artery

Answer 69

ABCDE emergency management - assess and stabilise patient Give IV mannitol if increased ICP Refer to neurosurgery - clot evacuation +/- litigation of bleeding vessel Maintain airway via intubation and ventilation in unconscious patient

Answer 70

Infection and inflammation of brain parenchyma

Answer 71

Most frequent in children and elderly - mainly viral caue | More common in immunocompromised

Answer 72

``` Mainly viral - Herpes simplex viruses 1 and 2 - Varicella zoster, EBV, cytomegalovirus, HIV, mumps, measles Non-viral - Bacterial meningitis - TB - Malaria ```

Answer 73

Extremes of age | Immunocompromised

Answer 74

Disease that mostly affects frontal and temporal lobes resulting in decreased consciousness, confusion and focal signs

Answer 75

Whole brain affected - problems with consciousness Insidious onset (days) or can be abrupt Triad - fever, headache, altered mental state Begins with features of viral infection - fever, headaches, myalgia, fatigue, nausea Progresses to - personality and behavioural changes, decreased consciousness, drowsiness, confusion Focal neurological deficit - hemiparesis, dysphasia, seizures, raised ICP, midline shift, coma Signs of meningitis Hx of travel and/or animal bite

Answer 76

Meningitis Stroke Brain tumour

Answer 77

MRI - Areas of inflammation and swelling, generally in temporal lobes in HSV encephalitis - May be midline shifting due to raised ICP Lumbar puncture - CSF shows elevated lymphocyte count - Viral detection by CSF PCR highly sensitive for herpes simplex and varicella zoster - False negative may occur within first 48 hours symptoms onset Blood and CSF serology usually helpful

Answer 78

If viral - immediate treatment with anti-viral IV acyclovir Early treatment can reduce mortality and long neuro damage Anti-seizure medication If meningitis suspected then emergency IM benzylpenicillin

Answer 79

Caused by reactivation of varicella zoster virus usually within dorsal root ganglia Primary infection with VZV causes chickenpox, following which the virus remains latent in sensory ganglia Development of shingles may indicate decline in cell-mediated immunity such as that due to age or malignancy

Answer 80

90% children have been exposed to chicken pox before 16 Can affect all ages but seen as disease of elderly Incidence and severity can increase with age Shingles cannot be caught from contact with person or chickenpox

Answer 81

``` Increasing age Immunocompromised HIV Hodgkin's lymphoma Bone marrow transplants ```

Answer 82

Viral infection affecting peripheral nerves When latent virus reactivated in dorsal root ganglia travels down affected nerve via sensory root in dermatomal distribution over period 3-4 days Results in perineural and intramural inflammation In immunocompromised, most frequent site is throacic nerves followed by ophthalmic division of trigeminal nerve Can also affect cervical, lumbar and sacral nerve roots Person with weeping shingles rash can cause chickenpox in non-immune person after close contact

Answer 83

Pain and paraesthesia in dermatomal distribution Rash for days Malaise, myalgia, headache, fever Rash - consists of papules and vesicles restricted to same dermatome - Neuritic pain - Crust formation and drying occurs over next week with resolution in 2-3 weeks - Patients infectious until lesions are dried - Rash doesn't extend outside dermatome

Answer 84

Before rash appears pain may come from chest or abdominal pain - cholecystitis or renal stones Cluster headaches/migraines Atopic eczema, contact dermatitis or herpes simplex or impetigo

Answer 85

Clinical diagnosis | Rash diagnostic

Answer 86

Oral antiviral therapy begun within 72 hours of rash onset - Oral acylovir x5 daily - Or oral valicilovir x2 daily - Or oral famciclovir x2 daily Rapid treatment to minimise risk of peripheral herpetic neuralgia Topical antibiotics treatment for secondary bacterial infection Analgesia eg ibuprofen for pain

Answer 87

``` Ophthalmic branch of trigeminal nerve - damage will affect sight Post herpetic neuralgia - Pain lasting for more than 4 months after developing shingles - Occurs in 10% patients often elderly - Burning, intractable pain - Responds poorly to analgesics Treat with - Tricyclic antidepressants - Anti-epileptics - Anti-convulsants ```

Answer 88

Inflammation of meninges

Answer 89

Occurs in people of all age groups but more common in infants, young children and elderly Meningococcal disease notifiable to PHE

Answer 90

Neisseria meningitides - gram negative diplococci transmitted by droplet spread Streptococcus pneumoniae/pneumoncoccus Less common H influenzae

Answer 91

Listeria monocytogenes - found in cheese

Answer 92

E coli | Group B haemolytic stretpcoccus - strep agalactiae

Answer 93

``` Cytomegalovirus Cryptococcus neoformans (fungi) TB HIV Herpes simplex virus ```

Answer 94

``` Intrathecal drug administration Immunocompromised Elderly Pregnant Bacterial endocarditis Crowding - military base, university students Diabetes Malignancy IVDU ```

Answer 95

Microorganisms reach meninges either by direct extension from ears, nasopharynx, cranial injury or congenital meningeal defect or bloodstream Immunocompromised patients at risk of infection with unusual organisms Acute bacterial meningitis - Typically sudden - Can lead to meningococcal septicaemia when bacteria invade blood - Presence of endotoxin leads to inflammatory cascade - Petechial rash and signs of sepsis - Pia arachnoid congested with polymorphs - Layer of pus which may organise to form adhesions causing cranial nerve palsies and hydrocephalus Chronic infection eg TB - Brain covered in viscous grey-green exudate with numerous meningeal tubercules Viral - Predominantly lymphcytic inflammatory CSF reaction without pus formation - Little or no cerebral oedema unless encephalitis develops

Answer 96

Triad - headache, neck stiffness, fever In acute bacterial - Onset sudden - Papilloedema bilateral occuring over hours-weeks - Intense malaise, fever, rigors, severe headache, photophobia, vomiting - Irritable and prefers to lie still - Neck stiffness, positive Kernig's and Brundzinski's sign - Meningococcal septicaemia - non-blanching petechial and purpuric rash - Altered mental state with high fever - Seizures and focal CNS signs - Progressive drowsiness, materialising signs, cranial nerve lesions indicate complication Viral meningitis - Benign, self-limiting condition lasting 4-10 days - Headache may follow for some months Chronic - TB - Long Hx and vague symptoms of headache, anorexia and vomiting - Sings of meningeal tried often absent/late

Answer 97

Aseptic meningitis due to tumour SAH Encephalitis

Answer 98

Blood cultures before lumbar puncture Blood tests - FBC, U&E, CRP, serum glucose Lumbar puncture - if unable to perform within 30 mins give empirical antibiotics - Send for microscopy and sensitivity - Can give headache, paraesthesia, CSF leak and damage to spinal cord CT head - To exclude lesions Throat swabs - bacterial and viral Pneumococal and meningococcal serum PCR

Answer 99

``` Bacteria - Neutrophil polymorphs - High protein - Low glucose TB - Lymphocytes - High protein - Low/normal glucose Viral - Lymphocytes - Normal protein - Normal glucose ```

Answer 100

IV benzylpenicillin or cefotaxime immediately Lumbar puncture not performed due to risk of coning and raised ICP Diagnosis confirmed by blood cultures

Answer 101

``` Age > 60 Immunocompromised Hx of CNS disease New onset/recent seizures Decreasing conscious levels GCS < 14 Focal neurological signs Papilloedema ```

Answer 102

Start antibiotics before tests come back if suspected IV cefotaxime or ceftriaxone If over 50/immunocompromised add IV amoxicillin to cover listeria Consider steroids to reduce cerebral oedema IV vancomycin if return traveller Prophylaxis for contacts - Oral ciprofloxacin stat - Oral rifampicin - cannot give when pregnant

Answer 103

Hearing loss Seizures Developmental problems

Answer 104

Impaired ability to move a body part in response to will | Weakness

Answer 105

Ability to move a body part in response to will completely lost

Answer 106

Incoordination | Willed movements clumsy, ill-directional or uncontrolled

Answer 107

Spontaneous movement of body part, indefinitely of will

Answer 108

Disorder of consciously organised pattern of movement or impaired ability to recall acquired motor skills

Answer 109

Located in anterior horns of spinal cord and in CN nuclei in brainstem

Answer 110

``` Motor nuclei of cranial nerves Motor neurones in spinal cord Spinal ventral roots Peripheral nerves Neuromuscular junction Muscle ```

Answer 111

Everything goes up Spasticity (increased muscle tone) Brisk reflexes Plantars upturned on stimulation - positive Babinski's sign Characteristic pattern of limb muscle weakness (pyramidal pattern) - Upper limbs extensor muscles weaker than flexors - Lower limb flexors weaker than extensors - Finer more skillful movement impaired

Answer 112

``` Everything goes down Muscle tone reduced - flaccid Muscle wasting Fasciculation - visible spontaneous contraction of motor units - not enough to diagnose LMN, need weakness too Reflexes depressed/absent ```

Answer 113

Cluster or major degenerative diseases charaterised by selective loss of neurones in motor cortex, cranial nerve nuclei and anterior horn cells

Answer 114

Relatively uncommon More common in men Median age onset 60 Often fatal in 2-4 years

Answer 115

``` Usually sporadic and of unknown cause No established factors 5-10% familial - Linked to mutation in free radical scavenging enzyme superoxide dismutase - Also linked to TDP-42, C9LRF72 and FUS ```

Answer 116

Degenerative condition affecting motor neurones, namely anterior horn cells Relentless and unexplained destruction of UMN and anterior horn cells in brain and spinal cord Causes both UMN and LMN dysfunction No sensory loss of sphincter disturbance Never affects eye movements Causes reactive oxygen species which damage DNA, lipids and proteins Most patients die within 3 years from respiratory failure as a result of bulbar palsy and pneumonia

Answer 117

Amyotrophic lateral sclerosis (UMN and LMN) - Weakness and UMN neurone signs - Split hand sign (thenar wasting, less hypothenar wasting) - Cramps - Wrist and foot drop Progressive muscular atrophy (LMN) - Weakness, muscle wasting, fasciculations - Affects distal before proximal Progressive bulbar palsy (LMN) - Lower CN 9-12 and nuclei - Dysarthria, dysphasia, nasal regurgitation (chocking) - LMN lesion of tongue and muscles of talking, swallowing, flaccid fasciculating tongue, jaw jerk normal/absent, speech quiet, hoarse of nasal Primary lateral sclerosis (LMN) - Loss of beta cells in motor cortex - UMN signs - No cognitive decline

Answer 118

> 40, stumbling spastic gait, foot drop +/- proximal myopathy, weak grip and shoulder abduction or aspiration pneumonia Frontotemporal dementia Spread of symptoms Rectal and bladder sphincters and oculomotor muscles spared No sensory symptoms

Answer 119

``` MS/polyneuropathies Myasthenia gravis Diabetic amyotrophy GBS Spinal cord tumour ```

Answer 120

Based on clinical findings - Definite - LMN and UMN signs in 3 regions - Probable - LMN and UMN in 2 regions - Probably with lab support - LMN and UMN signs in 1 region or UMN in more than one region + electomyography shows acute denervation in more than 2 limbs - Possible - LMN and UMN signs in 1 region - Suspected - LMN/UMN sign only in 1 or more Brain/spinal cord MRI (excludes structural causes) Lumbar puncture - excludes inflammatory causes Nerve conduction studies + electromyography Denervation of muscles due to degeneration of LMNs confirmed by EMG

Answer 121

Anti-glutametergic drugs - Oral riluzole (Na+ channel blocker inhibiting glutamate), prolongs life by 3 months - Raised LFTs so monitor - S/E vomiting, raised pulse, headache, vertigo Drooling - oral propantheline or amitriptyline Dysphasia - Blend food - Nasogastric tube - percutaneous catheter gastrostomy Spasms - oral baclofen Non-invasive ventilation if respiratory failure Analgesia - NSAIDs or opioids Specialist MDT supprot - neurologist, speech and language therapists, occupational therapist, specialist nurse, physiotherapise

Answer 122

Degenerative movement disorder caused by reduction in dopamine in substantia nigra Characterised by triad of rigidity, bradykinesia, resting tremor

Answer 123

Increasing prevalence with age Peak age of onset 55-65 More common in men

Answer 124

Idiopathic Drug induced Combination of - Environmental factors - pesticides, methyl-phenyl tetrahydropyridine in illegal opiates - Parkinson's genes - Oxidative stress and mitochondrial dysfunction

Answer 125

Male Increasing age FHx Being non-smoker have higher risk

Answer 126

Substania nigra produces dopamine Parkinson's results from mitochondrial dysfunction and oxidative stress Results from progressive degeneration of dopaminergic neurones from pars compacta of SN in midbrain that projects to striatum of basal ganglia Reduced striatal dopamine levels due to loss of dopaminergic neurones Less dopamine so thalamus inhibited resulting in decrease in movement Neuronal inclusions called Lewy-Bodies present in Parkinson's and become gradually more widespread as condition progresses, spreading from lower brainstem to midbrain and then cortex Degeneration of other basal ganglia nuclei Extent of nigrostriatal dopaminergic cell loss correlates with degree of akinesia

Answer 127

Onset gradual and often presents with impaired dexterity of unilateral foot drop Asymmetry Before motor symptoms - anosmia, depression/anxiety, aches and pains, REM sleep disorders, urinary urgency, hypotension, constipation Tremor - Worse at rest, asymmetrical, most obvious in hands, improved with voluntary movements, worsened by anxiety, 4-6 cycles/sec, issue with repetitive hand movements Rigidity - increased tone in limbs and trunk, limbs resist passive extension throughout movement, over entire radius of joint movement, can cause pain and problems with turning in bed Bradykinesia/hypokineaia - slow to imitate movement, reduce blink rate, monotonous hypophonic speech, smaller writing Gait - reduced asymmetrical arm swing, narrow gait, stooped posture and small steps, shuffling, narrow base Difficulty with fine movements Drooling and swallowing difficulty late Depression, constipation, increased urinary frequency

Answer 128

``` Benign essential tremor - worse on movement, rare at rest Multiple cerebral infarcts Lewy-body dementia Drug induced Wilson's disease Trauma All dopamine antagonists ```

Answer 129

Beta-blockers Primidone Gabapentin

Answer 130

Clinical Confirmation by response to L-dopa MRI head - initially normal but slowly shows atrophy, exclude tumours or normal pressure hydrocephalus If any of these present at beginning, sign probably not Parkinson's - Dementia, incontinence, symmetry, early falls

Answer 131

Compensate for loss of dopamine Explain disease slowly progressive and although incurable, amenable to palliation Balance problems, speech, gait disturbance don't respond to medication so physio Encourage physical activity Oral levodopa with decarboxylase inhibitor Doesn't alter disease progression, offers symptom relief Only started when absolutely necessary Dopamine agonists - oral ropinirole or pramiprexole Monoamine oxidase B inhibitors oral selefiline or rasagline Catechol-O-methyl transferase inhibitors eg oral entacapone or tolcapone Neuropsychiatric complications eg depression, dementia, psychosis Deep brain stimulation to help those who are partly dopamine responsive Surgical ablation of overactive basal ganglia circuits

Answer 132

Reduced efficacy over time even if dose increase On-dyskinesias Off-dyskinesias Freezing

Answer 133

Chronic autoimmune, T cell mediated inflammatory disorder of CNS in which there are multiple plaques of demyelination within brain and spinal cord, occurring sporadically over years Disease of CNS with oligodendroytes targeted, not schwann cells of PNS affects white matter of brain

Answer 134

``` Begins in early adulthood More common in women Presentation typically between 20-40 Presentation after 60 rare More common in white populations More common further from equator you go - rare in tropical countries ```

Answer 135

Relapsing and remitting - Most common pattern - Symptoms occur in attacks with onset over days and typically recovery either partial or complete over weeks - Periods of good health/remission followed by sudden symptoms or relapses - Patients may accumulate disability over time if don't fully recover from relapses Secondary progressive MS - Follows on from relapsing and remitting MS - Late stage of MS that consists of gradually worsening symptoms with fewer remissions - 75% patients with relapsing-remitting MS will eventually evolve into secondary progressive MS by 35 years after onset Primary progressive MS - Gradually worsening disability without relapses or remission - Typically presents later and associated with fewer inflammatory changes on MRI

Answer 136

Not understood Combination of genetic and environmental factors - Exposure to EBV in childhood - Low levels of sunlight and vitamin D

Answer 137

Female White Living far from equator - Southern and Northern hemispheres (vit D levels)

Answer 138

Autoimmune mediated demyelination at multiple CNS sites resulting in discrete plaques of demyelination affecting white matter Thought to be T cell mediated (activate B cells to produce auto-antibodies against myelin) Once T lymphocytes cross BBB cause destruction in brain Results in demyelination and thus conduction disruption along axons Although myelin sheath does regenerate, new myelin less efficient and temperature dependent - when exposed to high heat, conduction through new myelin decreases drastically Plaques of demyelination perivenular occur everywhere in CNS PNS not affected as Schwann cells unaffected due to different antigens Repeated demyelination leads to axonal loss and incomplete recovery between attacks Poor healing results in relapsing and remitting symptoms Multiple areas of sclerosis form along neurons slowing conduction of signals and impairing movement and/or sensations

Answer 139

``` Optic nerves Around ventricles of brain Corpus callosum Brainstem and cerebellar connections Cervical cord ```

Answer 140

In young adults 20-40 Monosymptomatic initially Symptoms may worsen with heat/exercise as new myelin inefficient and doesn't perform well in heat Unilateral optic neuritis - pain in one eye on movement, reduced central vision Numbness or tingling of limbs Leg weakness Brainstem demyelination - diplopia, vertigo, facial numbness/weakness, dysarthria/dysphasia Clumsy/useless hand or limb movements due to loss of proprioception Cerebellar symptoms such as ataxia Trigeminal neuralgia Constipation Spasticity and weakness Intention tremor Bladder dysfunction - urgency, frequency, incontinence Sexual dysfunction - erectile dysfunction Cognitive decline Amnesia

Answer 141

Hereditary spastic paraplegia Cerebral variant of SLE Sarcoidosis HIV

Answer 142

2/more attacks affecting different parts of CNS Exclude differentials with FBC, inflammatory markers, U&Es, LFTs, glucose, HIV serology, auto-antibodies, Ca2+, vitamin B12 MRI brain and cord - Diagnostic if Hx - 95% periventricular lesions - 90% discrete white matter abnormalities - Multiple scattered plaques usually seen Lumbar puncture - CSF exam shows oligoclonal IgG bands in over 90% cases - CSF cell count may be raised Electrophysiology - delayed nerve conduction suggests demyelination

Answer 143

Encourage stress-free life to help reduce number of lesions If poor diet and sun exposure give vit D Acute relapse - IV methylprednisolone for less than 3 days Frequent relapse - SC interferon 1B or 1A anti-inflammatory cytokines - Disease modifying agents - Monoclonal antibodies - IV alemtuzumab or IV natalizumab Symptomatic treatment of spasticity - Physio - Baclofen - Tizanidine - Botox injections - Urinary urgency and frequency - Incontinence Aggressive treatment - stem cell transplant Life expectancy for people with MS 5-10 years below average often die from aspiration pneumonia due to dysphagia and swallowing difficulties

Answer 144

Recurrent tendency to spontaneous, intermittent, abnormal electrical activity in part of brain, manifesting in seizures Ongoing liability to recurrent epileptic seizures Paroxysmal/unprovoked event in which changes of behaviour, sensation or cognitive processes are caused by excessive hypersynchronous neuronal discharged in brain Chronic disorder - need at least 2 seizures to be defined as epileptic

Answer 145

Motor signs of electrical discharges Many would have seizures in abnormal metabolic circumstances (hyponatraemia, hypoxia) But would not normally be said to have epilepsy

Answer 146

Common Incidence age-dependent, highest at extremes of life with most cases starting before 20 or after 60 Can often go into remission Seizures usually last 30-120 seconds

Answer 147

Primary generalised - Simultaneous onset of electrical discharge throughout whole cortex (involving both hemispheres), with no localising features referable to only one hemisphere - Bilateral symmetrical and synchronous motor manifestations - Always associated with loss of consciousness or awareness Partial/focal seizures - Focal onset, with features referable to a part of one hemisphere - Often seen with underlying structural disease - Electrical discharge restricted to a limited part of cortex of one cerebral hemisphere - May later become generalised eg secondary generalised tonic-clonic seizures

Answer 148

``` 2/3 idiopathic often familial Cortical scarring - Head injury years before onset - Cerebrovascular disease - CNS infection Space occupying lesion Tuberous sclerosis Alzheimer's or dementia Alcohol withdrawal ```

Answer 149

``` FHx Premature born babies who small for age Abnormal blood vessels in brain Alzheimer's or dementia Use of drugs Stroke/brain tumour/infection ```

Answer 150

Prodrome - Lasting hours or days may rarely precede seizures - Not part of seizure, results in change of mood or behaviour Aura - Part of seizure where patient aware and may precede other manifestation - Strange feeling in gut, deja vu or strange smells or flashing lights - Implies a partial (focal) seizure often not necessarily from temporal lobe Post-ictally (after) - Headache, confusion, myalgia, sore tongue - Temporary weakness after a focal seizure in motor cortex - Todd's palsy - Dysphasia following a focal seizure in temporal lobe

Answer 151

``` Generalised tonic-clonic seizure Typical absence seizure Myoclonic seizure Tonic seizure Atonic seizure ```

Answer 152

Simple partial seizure Complex partial seizure Partial seizure with secondary generalisation (Involves different lobes)

Answer 153

Often no aura Loss of consciousness Tonic phase - rigid, stiff limbs, falls to floor if standing Clonic phase - generalised, bilateral, rhythmic muscle jerking lasting secs-mins Eyes remain open, tongue often bitten Incontinence of urine/faeces Followed by period of drowsiness, confusion, coma for several hours

Answer 154

Usually disorder of childhood Child ceases activity, stares and pales for a few seconds Suddenly stops talking mid-sentence and then carries on where left off Often don't realise they had an attack On EEG - 3Hz spike and wave activity Tend to develop generalised tonic-clonic seizures later in life

Answer 155

Sudden isolated limb jerk, face or trunk | Patient suddenly thrown to ground, or have violently disobedient limb

Answer 156

Sudden sustained increased tone with characteristic cry/grunt Intense stiffening of body (tonic) Stiffening not followed by jerking

Answer 157

Sudden loss of muscle tone and cessation of movement resulting in fall

Answer 158

Not affecting consciousness or memory Awareness unimpaired with focal motor, sensory, autonomic or psychic symptoms No post-ictal symptoms

Answer 159

Affecting awareness of memory before, during or immediately after seizure Most commonly arise from temporal lobe Post-ictal confusion common with seizures arising from temporal lobe whereas recovery rapid after seizure in frontal lobe

Answer 160

Electrical disturbance starts focally (as either simple or complex partial seizure) then spreads widely causing a secondary generalised seizure which is convulsive

Answer 161

Aura Anxiety or out of body experience Automatisms eg lip smacking, chewing, fiddling

Answer 162

Motor features such as posturing or peddling movements of leg Jacksonian March - seizure moves up and down motor homunculus starting at face/thumb Post-ictal Todd's palsy

Answer 163

Sensory disturbances - tingling/numbness

Answer 164

Visual phenomena eg spots, lines or flashes

Answer 165

``` Tongue biting Head turning Muscle pain Loss of consciousness Cyanosis Post-ictal symptoms ```

Answer 166

Prolonged upright position Sweat prior to loss of consciousness Nausea

Answer 167

Non-epileptic seizures are situational Longer, closed mouth/eyes during tonic-clonic movements, pelvic thrusting Do not result from sleep, no incontinence or tongue biting Pre-ictal anxiety symptoms in non-epileptic seizure

Answer 168

``` Postural syncope Cardiac arrhythmia TIA Migraine Hyperventilation Hypoglycaemia Panic attacks Non-epileptic seziure ```

Answer 169

At least 2 or more unprovoked seizures occurring > 24 hours apart EEG - not diagnostic - Performed to support diagnosis - Helps to determine type of seizure and what epilepsy syndrome - Frequently normal between attacks and false-positive may be detected in non-epileptics MRI - With imaging of hippocampus CT head - Used in emergency to look for space occupying lesion - Used to identify or exclude abnormalities that could be causing symptoms Bloods - FBC, electrolytes, Ca2+, renal function, liver function, urine biochemistry, blood glucose levels - Rules out metabolic causes Genetic testing

Answer 170

Emergency measures - ABCDE - Check glucose - Prolonged seizure or repeated seizures treated with rectal/IV diazepam or lorazepam - IV phenytoin loading - If still fitting then anaesthetist involvement for anaesthetic and ventilation Generally drugs not advised after one fit unless risk of recurrence high Resistant to drug treatment in 1/3 patients Possible drug treatments - Oral sodium valproate - Oral lamotrigine - Oral carbamazepine

Answer 171

Compression of spinal cord resulting in UMN signs and specific symptoms depending on where compression is

Answer 172

Vertebral body neoplasms - most common - Secondary malignancy commonly from lung, breast, prostate, myeloma and lymphoma Spinal pathology - Disc herniation - nucleus pulposus moved out through annulus resulting in pressure on nerve root and pian - Disc prolapse - nucleus pulosus presses against annulus Rarer - infections, haematoma, primary spinal cord tumour

Answer 173

Spinal or root pain may precede leg weakness and sensory loss Progressive weakness of legs with UMN signs Onset may be acute or chronic depending on cause Arm weakness often less severe Bladder sphincter involvement late and manifests as hesitancy, frequency, and later as painless retention Sensory loss below level of lesion Look for motor, reflex and sensory level with normal findings above level of lesion LMN signs at level and UMN below level Depends on level of lesion L5/S1 sciatica

Answer 174

``` Transverse myelitis Multiple sclerosis Cord vasculitis Trauma Dissecting aneurysm ```

Answer 175

Imaging (don't delay) - irreversible paraplegia may follow if cord not decompressed Speed of imaging should be parallel to rate of clinical progression MRI - gold standard - identifies cause and site Biopsy/surgical exploration to identify masses Blood tests - FBC, ESR, B12, U&Es, syphilis serology, LFT, PSA CXR - if TB or malignancy

Answer 176

If malignancy - IV dexamethasone to reduce inflammation and oedema around malignancy and consider chemo/radiotherapy Epidural abscess - surgically decompressed and antibiotics Refer to neurosurgeons - Epidural steroid injection for leg pain - Surgical decompression of cord - Laminectomy - removal of lamina/spongy tissue between discs to relieve pressure - Microdiscectomy - removal of herniated tissue from disc

Answer 177

Medical emergency Cauda equina formed by nerve roots caudal to level of termination of spinal cord at L1/2 Spinal damage caudal to L1 Flaccid and areflexic weakness

Answer 178

Rare, occurring mainly in adults but can occur at any age | Common cause - lumbar disc herniation at L4/5 and L5/S1

Answer 179

``` Herniation of lumbar disc Tumours/metastases Trauma Infection Spondylolisthesis Post-op haematoma ```

Answer 180

Major different between cauda equina and lesions higher up - leg weakness is flaccid and areflexic (LMN) Sciatic pain, numbness, tingling sensation that radiates from lower back and travels down one of legs to foot and toes Bilateral sciatica Saddle anaesthesia Bladder/bowel dysfunction Erectile dysfunction

Answer 181

Conus medullaris syndrome Vertebral fracture Peripheral neuropathy Mechanical back pain

Answer 182

``` MRI to localise lesion Knee flexion to test L5-S1 Ankle plantar flexion - test S1-2 Straight leg raising - L5 -S1 root problem Femoral stretch test - L4 root problem ```

Answer 183

Refer to neurosurgeon ASAP to relieve pressure or risk irreversible paralysis/sensory loss/incontinence - Microdisectomy - Epidural steroid injection - Surgical spine fixation - Spinal fusion

Answer 184

Disorders of peripheral or cranial nerves, whose distribution is usually symmetrical and widespread Often with distal weakness and sensory loss - glove and stocking

Answer 185

``` By course - acute/chronic By function - sensory/motor/autonomic/mixed By pathology - demyelination/axonal degeneration/both Mostly motor - GBS - Lead poisoning - Charcot-Marie-Tooth syndrome Mostly sensory - DM - Renal failure - Leprosy ```

Answer 186

Metabolic - DM, renal failure. hypothyroidism, hypoglycaemia Vaculitides - polyarteritis nodsa, rheumatoid arthritis, Wegner's granulamatosis Malignancy - paraneoplastic syndrome, polycythaemia rubra vera Inflammatory - GBS, sarcoidosis Infections - leprosy, HIV, syphilis, Lyme disease Nutritional - decreased Vit B12, B1, E, B6, folate Inherited syndromes - Charcot-Marie-Tooth, porphyria Drugs/toxins - lead, arsenic, alcohol, vincristine, cisplatin, metronidazole

Answer 187

Numbness, paraesthesia Affects extremities first - glove and stocking Difficulty handling small objects such as buttons Signs of trauma eg burns or joint deformation Diabetic and alcoholic neuropathies typicalyl painful

Answer 188

Often progressive - may be rapid Weak or clumsy hands Difficulty walking - falls and stumbling Difficulty breathing - reduced vital capacity LMN lesion - wasting and weakness most marked in distal muscle of hands and feet Reflexes are reduced/absent

Answer 189

Hx vital - be clear about time course, precise nature of symptoms and any preceding or associated events - Diarrhoea and vomiting before GBS - Weight loss in cancer - Arthralgia from connective tissue disease Ask about travel, alcohol and drug use, sexual infections and FHx If palpable nerve thickening - leprosy or Charcot-Marie-Tooth Examine other systems for clues to causes FBC, ESR, glucose, U&Es, LFT, TSH, B12 ANA, ANCA, anti-CCP CXR Urinalysis Lumbar puncture and specific genetic testing for inherited neuropathies

Answer 190

Treat cause Foot care and shoe choices important to minimise trauma in sensory Splinting of joints help prevent contractures in prolonged paralysis For vasculitis causes - steroids, immunosuppressants Treat neuropathic pain with oral amitriptyline or oral nortirptyline

Answer 191

Acute inflammatory demyelinating ascending polyneuropathy affecting the peripheral nervous system following an upper respiratory or GI tract infection

Answer 192

More common in men Peak ages 15-35 years and 50-75 years Most common acute polyneuropathy

Answer 193

``` Campylobacter jejuni Cytomegalovirus Mycoplasma Zoster HIV EBV In some cases, no obvious infection can be found ```

Answer 194

History of respiratory GI infections 1-3 weeks prior to onset Vaccinations have been implicated Post-pregnancy - incidence decreases during pregnancy but increase in months after delivery

Answer 195

Usually triggered by infection Thought that infectious organisms share same antigens as those Schwann cells such as ganglioside GM and GQ1b leading to autoantibody mediated nerve cell damage formation via molecular mimicry Nerve cell damage consists of damage to Schwann cells and thus demyelination resulting in reduction in peripheral nerve condition resulting in an acute polyneuropathy

Answer 196

1-3 weeks post infection as symmetrical ascending muscle weakness starts - may advance quickly, affecting all limbs at once and can lead to paralysis Proximal muscles more affected eg trunk, respiratory, cranial nerves In 20% respiratory muscles and facial muscles are affected - respiratory involvement required ITU admission Pain common eg back and limb Sensory signs include paraesthesia by very few sensory signs Reflexes lost early in illness Autonomic features such as sweating, raised pulse, BP changes, arrhythmias may be present Progressive phase of up to 4 weeks, followed by recovery

Answer 197

Other causes of acute paralysis - Hypokalaemia - Stroke - Brainstem compression - Encephalitis - Spinal cord compression - Poliomyelitis - Vasculitis - Myasthenia gravis

Answer 198

Nerve conduction studies - Diagnostic if matches with clinical exam - Shows signs of conduction, prolonged distal motor latency +/- conduction block Lumbar puncture at L4 - CSF has raised protein but normal WCC Spirometry - To monitor FVC if there is respiratory involvement - Decreased FVC indicated need to admit to ITU to maintain airways

Answer 199

If FVC < 1.5L/80% then ventilated and admit to ITU - monitor FVC 4 hourly IV immunoglobulins for 5 days - Decreases duration and severity of paralysis - Contraindicated in patients with IgA deficiency (can cause allergic reaction) Plasma exchange LMW heparin and compression stockings to reduce risk of venous thrombosis Prognosis good with 85% making complete/near complete recovery 105 unable to walk alone at 1 yr Mortality 10%

Answer 200

Autoimmune disease against nicotinic acetylcholine receptors in neuromuscular junction

Answer 201

More common in women - although over 50 more common in men Peak age of incidence at 30 in women Peak age of incidence at 60 in men

Answer 202

If under 50 and MG commoner in women - associated with other autoimmune disease If over 50 and MG commoner in men, associated with thymic atrophy or thymic tumour, RA and SLE Transient MG sometimes caused by D-penicillamine treatment for Wilson's disease

Answer 203

Autoimmune disease mediated by antibodies to nicotinic acetylcholine receptor - anti-AChR antibodies interfering with neuromuscular junction via depletion of working post-synaptic receptor sites Achieved by immune complex deposition of anti-AChR IgG and complement at post-synaptic membranes, causing interference and destruction of receptors Both B and T cells are implicated Blocks the excitatory effect of ACh on nicotinic receptors resulting in muscle weakness - results in less nicotinic receptors

Answer 204

Increasing muscular fatigue Muscle groups affected in order - Extra-ocular - Bulbar - Face - Neck - Trunk Limb muscles, speech and facial expression commonly affected Look for ptosis, diplopia and myasthenic snarl on smiling Respiratory difficulties can occur in generalised myasthenia Tendon reflexes are normal but may be fatiguable On examination to elicit fatiguability - Ask patient to count to 50 (becomes less audible) - Hold finger up high and ask patient to keep looking at it without lifting head up - after a few seconds, unable to keep eyes raised Weakness worsened by pregnancy, hypokalaemia, infection, emotion, exercise and drugs - opiates, beta-blockers, gentamycin and tetracycline

Answer 205

MS Hyperthyroidism Acute GBS Lambert-Eaton myastheic syndrome - Paraneoplastic condtion, most often seen with small cell lung cancer - Causes defective ACh release at neuromuscular junction resulting in proximal limb weakness with some absent reflexes - Weakness tends to improve after exercise unlike MG

Answer 206

Serum anti-AChR - raised in 90%, if negative then look for MuSK antibodies Electromyography and nerve conduction study - EMG will detect MG, detect electrical activity from muscles, characteristic decrement occurs in evoked muscle action potential during repetitive stimulation CT of thymus to look for hyperplasia, atrophy or tumour Ptosis improves by < 2mm after ice application to shut affected lid for > 2 mins - nice non-invasive cheap test Tensilon test - IV edrophonium given and muscle power increases within seconds - rarely used due to side effects

Answer 207

Symptom control - Anti-cholinesterase so more ACh remains in neuromusclar junction (also increased salivation, lacrimation, sweats, vomiting, miosis, diarrhoea) Immunosuppression - Used to treat relapses or if there is no response to pyridostigmine start low dose of steroids with dose increased per week - reduce dose on remission - Steroids may be combined with oral azathioprine or methotrexate as disease becomes general Thymectomy - removal of thymus in onset < 50 and disease poorly controlled with anti-cholinesterases

Answer 208

Weakness of respiratory muscle during relapse can be life-threatening Monitor FVC Treat with plasmapheresis and IV immunoglobulin and identify and treat trigger of relapse eg infection, medications

Answer 209

Pathological process affecting a peripheral nerves

Answer 210

Process affecting a single nerve

Answer 211

Several individual nerves affected

Answer 212

Diffuse, symmetrical disease usually commencing peripheral Can be motor, sensory, sensorimotor and autonomic Classified into demyelinating and axonal types Widespread loss of tendon reflexes typical, with distal weakness and distal sensory loss

Answer 213

``` Demyelination Axonal degeneration Compression Infarction Infiltration Wallerian degeneration ```

Answer 214

Schwann cell damage leads to myelin sheath distribution | Results in marked slowing of conduction seen in GBS

Answer 215

Axonal damage causes nerve fibre to die back from periphery Conduction velocity initially remains mortal because of axonal continuity maintained in surviving fibres Axonal degeneration typically occurs in toxic neuropathies

Answer 216

Focal demyelination at point of compression causes disruption of conduction Typically occurs in entrapment neuropathies eg carpal tunnel syndrome

Answer 217

Micro-infarction of vasa nervorum occurs in diabetes and arteritis such as polyarteritis nodosa and eosinophilic gransulomatosis with polyangitis

Answer 218

Occurs by inflammatory in leprosy and granulomas such as sarcoid and by neoplastic cells

Answer 219

Process that results when a nerve fibre is cut or crash and distal part of axon that is separated from neurones cell body degenerates

Answer 220

``` WARDS PLC Wegner's granulomatosis AIDS/Amyloid Rheumatoid arthritis Diabetes mellitus Sarcoidosis Polyarteritis nodosa Leprosy Carcinoma Carpal tunnel syndrome most common mononeuropathy ```

Answer 221

Usually local causes such as trauma, entrapment (tumour)

Answer 222

Most common mononeuropathy and entrapment neuropathy | Results from pressure and compression on median nerve as it passes through the carpal tunnel in wrist

Answer 223

More common in women as they have narrower wrists but similar sized tendons to men

Answer 224

``` Idiopathic Usually in those over 30 Associated with - Hypothyroidism - DM - Pregnancy (third trimester) - Amyloidosis including dialysis patients - Obesity - Rheumatoid arthritis - Acromegaly ```

Answer 225

Intermittent and gradual onset Aching pain in hand and arm (especially at night) can wake patient up Paraesthesiae in thumb, index, middle and half ring finger and palm Relieved by dangling hand over the edge of the bed - wake and shake May be sensory loss and weakness of abductor pollicis brevis +/- wasting of thenar eminence Light touch, 2-point discrimination and sweating may be impaired

Answer 226

Peripheral neuropathy Motor neurone disease MS

Answer 227

Electromyography - See slowing of conduction velocity in median sensory nerves across carpal tunnel - Prolongation of median distal motor latency - Helps confirm lesion site and severity Phalen's test - can only maximally flex wrist for 1 minute Tinel's test - tapping on nerve at wrist induces tingling (non-specific)

Answer 228

Wrist splint at night Local steroid injection Decompression surgery - carpal tunnel ligament cut to reduce pressure

Answer 229

Sympathetic or parasympathetic neuropathies may be isolated or part of generalised sensorimotor peripheral neuropathy

Answer 230

``` DM GBS Sjorgren's HIV SLE ```

Answer 231

Postural hypotension - faints on standing, eating or hot bath Ejaculatory failure Reduced sweating

Answer 232

Erectile dysfunction Constipation Nocturnal diarrhoea Urine retention

Answer 233

``` Tumour MS Trauma Aneurysm Vertebral artery dissection resulting in infarction Infection - cerebellar abscess from ear ```

Answer 234

Oculomotor Ptosis Fixed dilated pupil due to loss of parasympathetic outflow from Ediger-Westphal nucleus which supplies pupillary sphincter and ciliary bodies - lens accomodation Eye down and out Causes - raised ICP, diabetes, hypertension, giant cell arteritis

Answer 235

Trochlear Innervated superior oblique muscle and results in head tilt to correct extortion that results in diplopia and looking down Caused by trauma to orbit

Answer 236

Abducens Adducted eye Causes - MS, Wernicke's encephalopthy, pontine stroke (presents with fixed small pupils +/- quadriparesis

Answer 237

Non-function eye | Causes - stroke, tumours, Wernicke's encephalopathy

Answer 238

Trigeminal Jaw deviated to side of lesion Loss of corneal reflex Causes - trigeminal neuralgia (pain but no sensory loss), herpes zoster, nasopharyngeal cancer

Answer 239

Facial Facial droop and weakness Causes - Bells palsy most common lesion of facial nerve, fractures of petrous bone, middle ear infections, inflammation of parotid gland

Answer 240

Vestibulocochlear Hearing impairment Vertigo and lack of balance Causes - vestibulocochlear nerve runs very close to bone, very affected by surrounding tumours, skull fractures, toxic drug effects, ear infections

Answer 241

``` Glossopharyngeal and vagal Gag reflex issues Swallowing issues Vocal issues Caused by jugular foramen lesion ```

Answer 242

Incidence of 8 per 100,000 16th most common adult cancer - disproportionate killer in young adults 2nd most common paediatric cancer Account for less than 2% of all malignant tumours but 20% of childhood In adults, majority supratentorial In children - majority occur in posterior fossa Majority are gliomas - Astrocytoma (85-90%) - Oligodendroglioma (5%)

Answer 243

``` More common in affluent groups Ionising radiation Vinyl chloride Immunosuppression FHx ```

Answer 244

Grade I - good prognosis, often completely benign Grade II - > 5 year pronosis, premalignant tumour Grade III - prognosis of 2-5 year survival, cancer, malignant, active growth and mitotic acitivty Grade IV - < 1 year survival prognosis, most common phenotype, active growth, mitotic activity and necrosis, vascular proliferation, very malignant

Answer 245

Given enough time, all gliomas will progress to become glioblastoma multiforme except pliocytic astyocytoma (grade I) Common pathway - Especially in those under 50-60 - Initial genetic error of glucose glycolysis - Mutation of isocitrate dehydrogenase I - Results in excessive build-up of 2-hydroxyglutarate - Triggers genetic instability in glial cells and subsequent inappropriate mitosis leading to cancer Less common pathway - More common in those over 50-60 - No IDH-1 mutation - Resulting in very poor prognosis even for low grade tumours

Answer 246

``` Most common in 40s-50s Arise from oligodendrocytes Grow slowly, usually over several years Calcification is common May have seizures WHO grade II All are IDH-1 mutation positive ```

Answer 247

Arise from ependymal cells | Line ventricles and spinal cord

Answer 248

More common in older people and women | Benign and arise from arachnoid mater and may grow to a large size, usually over years, pushing into the brain

Answer 249

Solid benign tumours that arise from Schwann cell and occur principally in cerebellopontine angle

Answer 250

Very rare benign tumours | Often diagnosed in younger patients

Answer 251

Intracranial compartment is a complaint system Initially when tumour is small, there will be no symptoms despite the rising ICP - due to brain compliance and ability to remove CSF from ventricle to spinal cord in order to offset the increase in pressure Comes to a point where no more CSF can be relocated leading to a very sharp rise in ICP resulting in symptoms Rising pressure results in midline shift of brain and herniation through foramen magnum

Answer 252

Symptoms of raised ICP - Progressive headache - worse on waking from sleep, pain so bad can wake up, increased by coughing, straining and bending forwards, sometimes relieved by vomiting - Drowsiness - +/- vomiting - Papilloedema Progressive neurological deficit depending on part of brain affected - Temporal - dysphasia, amnesia - Frontal lobe - hemiparesis, personality change, Broca's dysphasia, lack of initiative, unable to plan tasks Parietal lobe - hemisensory loss, reduction in 2-point discrimination, dysphasia, astereognosis Occipital lobe - contralateral visual defects Cerebellum - DASHING - Dysdiadochokinesis, Ataxia, Slurred speech, Hypotonia, Intention tremor, Nystagmus, GGait abnormality Epilepsy/seizure of recent onset, partial/focal seizures more common Lethargy/tiredness caused by pressure on brainstem

Answer 253

``` Aneurysm Abscess Cyst Haemorrhage Idiopathic intracranial hypertension ```

Answer 254

CT and MRI - MRI superior for posterior fossa lesions - Determine size and location - High grade tumours have irregular edges and high growth rate Bloods - FBC, U&Es, LFTs, B12 Biopsy - Via skull burr-hole - To determine cancer grade and confirm Lumbar puncture contraindicated when possibility of mass lesion since withdrawing CSF my provoke immediate coning

Answer 255

Surgery to remove mass if possible Chemotherapy for glioma - at same time as surgery than 6 weeks post-op, temozolomide, not all tumours sensitivie due to methyl-guanine-methyl-transferase - If it has methylated MGMT then sensitive Oral dexamethasone to reduce inflammation and oedema Anti-convulsants

Answer 256

``` 10x more common than primary brain tumours Commonest neoplasms to metastasise to CNS in order - Non-small cell lung - Small cell lung - Breast - Melanoma - Renal cell - GI ```

Answer 257

Surgery if < 75 years Radiotherapy Chemotherapy Palliative therapy

Answer 258

Cause of chorea | Neurodegenerative disorder characterised by lack of inhibitory neurotransmitter GABA

Answer 259

Continuous flow of jerky, semi-purposeful movements, flitting from one part of the body to another They may interfere with voluntary movements but cease during sleep

Answer 260

Autosomal dominant condition with full penetrance Incurable, progressive neurodegenerative disorder Presents in middle age initially with a prodromal phase of mild symptoms eg irritability, depression and inco-ordination then progressing to psychiatric and cognitive symptoms Very rare Prevalence worldwide 5 per 100,000

Answer 261

Mutation on chromosome 4 | Resulting in repeated expression of CAG sequence

Answer 262

FHx | Having a parent with Huntington's child has 50% risk of getting it

Answer 263

Repeated expression of CAG sequence leads to translation of expanded polyglutamine repeated sequence in Huntington's gene Protein gene product function in unclear - expansion thought to be a toxic gain of function mutation More CAG repeats present earlier symptom present - Most adult onset have 36-55 repeats - Early onset 60 Progressive cerebral atrophy with marked loss of neurones in caudate nucleus and putamen of basal ganglia - loss of gaba-nergic and cholinergic neurones Results in decreased ACh and GABA synthesis in striatum GABA main inhibitory neurotransmitter, loss of this will result in decreased inhibition of dopamine release therefore resulting in excessive thalamic stimulation and thus excessive movements

Answer 264

Prodromal phase of mild psychotic and behavioural symptoms Chorea - Relentlessly progressive, jerky, explosive, rigidity involuntary movements - ceases when sleeping - Can't sit still - Begin as general restlessness, unintentionally initiated movements and lack of co-ordination Dysarthria, dysphagia, abnormal eye movements Psychiatric movements - Behavioural change -aggression, addictive behaviour, apathy, self-neglect - Depression/anxiety Dementia Associated with seizures Eventually death - usually occurs within 15 years of diagnosis, usually from an intercurrent illness

Answer 265

Other causes of chorea - Sydenham's chorea (rheumatic fever) - Creutzfeldt-Jakob disease - Wilson's disease - SLE - Stroke of basal ganglia

Answer 266

Diagnosis mainly clinical Genetic testing - many CAG repeats Extensive genetic counselling required due to impact a positive diagnosis CT/MRI showing caudate nucleus atrophy and increased size of frontal horns of lateral ventricles - Imaging not useful early on

Answer 267

No treatment to prevent progression Counselling to patient and family, genetic counselling to children of patients Symptomatic management of chorea - Benzodiazepines, sulpiride (neuroleptic to depress nerve function), tetradenazine Anti-depressants such as SSRIs Antipsychotic medication such as neuroleptics To treat aggression use risperidone

Answer 268

Syndrome caused by a number of brain disorders which cause memory loss, difficulties with thinking, problem solving or languages as well as difficulties with activities of daily living Alzheimer's most common Specific symptoms depend on parts of brain damaged and disease causing dementia

Answer 269

Rare under 55 Prevalence rises with age AD more common in women Vascular and mixed dementia more common in men

Answer 270

Alzheimer's disease (50%) - Most common - Degeneration of cerebral cortex, with cortical atrophy - Accumulation of beta-amyloid peptide, degeneration product of amyloid precursor protein, results in progressive neuronal damage, neurofibrillary tangles, increases in number of amyloid plaques and loss of ACh Vascular dementia (25%) - Brain damage due to CVS disease - Signs of vascular pathology Lewy-body dementia (15%) - Deposition of abnormal protein within neurons in brain stem and neocortex - Presents with fluctuating cognitive impairment, details visual hallucinations - Associated with Parkinson's Fronto-temporal dementia - Specific degeneration or atrophy of frontal and temporal lobes of brain - Behavioural and personality change, early preservation of episodic memory and spatial orientation, emotional unconcern, lowers inhibition Mixed dementia Parkinson's dementia Huntington's Liver failure HIV Prion disease Vitamin B12/folate deficiency

Answer 271

``` FHx Age Down's syndrome Alcohol use, obesity, high BP, hypercholesterolaemia Diabetes Atherosclerosis Depression High oestrogen levels ```

Answer 272

25% of all patients with AD with develop Parkinson's

Answer 273

Insidious onset with steady progression over years Short-term memory loss usually most prominent early symptoms, subsequently slow disintegration of personality and intellects Eventually affects all aspects of cortical function Decline in language, visuospatial skills, apraxia, agnosia

Answer 274

Stepwise deterioration with declines followed by periods of stability History of TIAs and/or strokes Evidence of atheropathy

Answer 275

Fluctuating cognition with pronounced variation in attention and alertness Prominent or persistent memory loss may not occur in early stages Impairment in attention, frontal, subcortical and visuospatial ability often prominent Depression and sleep disorders occur Visual hallucinations Parkinson's Loss of inhibitions

Answer 276

Substance abuse Hypothyroidism Space-occupying intracranial lesions Huntington's

Answer 277

Hx MMSE - score of 25/30 normal, 18-24 mild-moderate, 17 or below Exclusion of rare treatable causes of dementia should be considered Blood tests - FBC, liver biochemistry, TFTs, vitamin B12/folate Neuropsychology Brain CT in younger patients or those with atypical presentation MRI - extent of atrophy Brain function assessed - Energy and blood supply via PET and SPECT scanning - Brain networks via functional MRI

Answer 278

No specific therapy Support - Socially active - talking to family and friends - Cognitively acitve - Specialist memory service Carers Medication - Acetylcholinesterase inhibitor in Alzheimer's to increased ACh - BP control to reduce further vascular damage

Answer 279

Health behaviours Smoking cessation, good diet, physical activity and low alcohol Engaging in more than 6 leisure activities Education, occupation, premorbid IQ, mental acitivities decreases risk Changes in CSF amyloid-beta seen 25 years before onset of symptoms

Answer 280

Chronic, debilitating condition resulting in intense and extreme episodes of pain

Answer 281

``` Peak incidence between 50-60 years More common in women Prevalence increases with age May be due to genetic disposition Almost always unilateral ```

Answer 282

Compression of trigeminal nerve by loop of vein or artery Local pathology - aneurysms, meningeal inflammation, tumours 5th nerve lesion due to pathology - Within brainstem - tumour, MS, infarction - At cerebellopontine nagle - acoustic neuroma, another tumour - Within petrous bone - spreading middle ear infection - Within cavernous sinus - aneurysm of internal carotid, tumour or thrombosis of cavernous sinus

Answer 283

Hypertension main risk factor | Triggers - washing affected area, shaving, eating, talking and dental prostheses

Answer 284

Compression of trigeminal nerve resulting in demyelination and excitation of nerve resulting in erratic pain signalling

Answer 285

Almost always unilateral At least 3 attacks of unilateral facial pain Facial pain occurs in one or more distributions of trigeminal nerve, with no radiation beyond trigeminal distribution Pain has at least 3 of following - Reoccuring in paroxysmal attacks from a fraction of a second to 2 minutes - Severe intensity - Electric shock like, shooting, stabbing or knife-like - Precipitated by innocuous stimuli by affected side of face

Answer 286

Giant cell arteritis Temporal arteritis Dental pathology Temporomandibular joint dysfunction, migraine, cluster headaches

Answer 287

Needs to be at least 3 attacks with unilateral facial pain Clinical diagnosis based on criteria above and based on Hx MRI to exclude secondary causes or other pathologies Not attributes to another disorder

Answer 288

``` Typical analgesics and opioids do not work Anticonvulsants Less effective options May spontaneously remit after 6-12 months If drugs fail then surgery - Microvascular decompression - Gamma knife surgery - Stereotactic radiosurgery ```

Answer 289

C6-T1 Wrist lesions - due to lacerations/carpal tunnel Weakness of abductor pollicis brevis and sensory loss over radial 3.5 fingers and palm

Answer 290

C7-T1 Vulnerable to elbow trauma Compression occurs at epicondylar groove or at point where nerve passes between 2 heads of flexor carpi ulnaris Signs - Weakness/wasting of medial wrist flexors, interossi, medial 2 lumbricals - Wasting on hypothenar eminence, weak little finger abduction - Sensory loss over medial 1.5 fingers and ulnar side of hand - Flexion of 4th and 5ht DIP weak - With lesion at wrist, claw hand more marked Treatment - Rest and avoiding pressure on nerve - Night time soft elbow splint

Answer 291

C5-T1 Nerve opens to fist Damaged by compression against humerus Signs - Test for wrist and finger drop with elvow flexed and arm pronated - Sensory loss variable - dorsal of root of thumb most reliably affected BEST - Brachioradialis, extensors, supinator, triceps

Answer 292

Pain/paraestheisa and weakness in affected arm in variable distribution Causes - Trauma, radiotherapy for breast carinoma, prolonged wearing of heavy rucksack, neuralgic amyotrophy, thoracic outlet compression

Answer 293

Orthopnoea with raised hemidiaphragm on CXR Causes - lung cancer, myeloma, thymoma, cervical spondylosis, trauma, phrenic nucleus lesion, thoracic surgery, C3-5 zoster, HIV, muscular dystrophy

Answer 294

Meralgia paraesthetica Antero-lateral burning thigh pain from entrapment under inguinal ligament L2-3

Answer 295

L4-S3 Damaged by pelvis tumours or fractures to pelvis or femur Lesions affect hamstrings and all muscles below knee Foot drop Loss of sensation below knee laterally

Answer 296

L4-S1 Originates from sciatic nerve just above knee Often damaged as it winds around fibular head due to trauma or sitting cross legged Foot drop Weak ankle dorsiflexion Eversion Sensory loss over dorsum of foot

Answer 297

L4-S3 Originates from sciatic nerve just above knee Lesions lead to an inability to stand on tiptoe, invert foot or flex toes Sensory loss over sole

Answer 298

``` GCS up to 14 score - Motor response - Verbal response - Eye opening response Inaccurate within 1 hour of event Lateralising signs - identifies which hemisphere issue is in, check painful stimuli response Look for pupils for signs of raised ICP ```

Answer 299

``` IV mannitol (diuretic to reduce oedema) Management of seizures Monitor vital signs Intubation if GCS < 8 Neurosurgery - ICP monitor insertion, Burrholes or craniotomy to relieve ICP Suture scalp lacerations before CT ```

Answer 300

``` Congenital ataxias Diseases where ataxia is one of many features Episodic ataxia Autosomal recessive ataxia - Friedreich's ataxia Autosomal dominant ataxia - Spinocerebellar ataxia 6 Sporadic ataxia - Gluten ataxia - Toxic effects ```

Answer 301

Purkinje layer as only output | Results in dysfunction and ataxia

Answer 302

``` Dysarthria Dysphagia Clumsiness Intention tremor Unsteadiness when walking Stumbling and falls Cognitive problems Nystagmus Limb and gait ataxia ```

Answer 303

MRI to look for - Cerebrovascular damage - Primary tumours - Secondary tumours - Hydrocephalus - MS

Answer 304

Hemi-section of spinal cord | Ipsilateral and contralateral are in relation to lesion

Answer 305

Ipsilateral weakness below lesion - damage of ipsilateral descending motor tracts Ipsilateral loss of dorsal column proprioception below lesion - ascending tracts damaged before they could decussate Contralateral loss of spinothalamic pain and temperature

Answer 306

Opioid effects and some serotonin reuptake inhibition | Class 3a controlled drug

Answer 307

Citalopram Fluoxetine Sertraline

Answer 308

First line treatment for moderate to severe depression and in mild depression if other treatments fail Panic disorder or OCD

Answer 309

Preferentially inhabit neuronal reuptake of serotonin from synaptic cleft so increase availability for neurotransmission Improves mood and physical symptoms of depression and relieves symptoms of panic

Answer 310

GI disturbance, appetite, weight disturbance, hypersensitivity reactions Hyponatraemia Suicidal thoughts/behaviours may increase Lowers seizure thresholg Prolonged QT Use with care in people with peptic ulcers, epilepsy, hepatic impairment, may not be effective in young people CI with other monoamine oxidase inhibitors as may cause serotonin syndrome CI with other drugs that prolong QT May also increase bleeding when used with anticoagulants

Answer 311

Amitriptyline

Answer 312

Second line treatment for moderate to severe depression where SSRIs are ineffective

Answer 313

Inhibit neuronal uptake of serotonin and noradrenaline from synaptic cleft so increase availability Improves mood and physical symptoms Blocks wide range of receptors accounting for range of side effects

Answer 314

Dry mouth, constipation, urinary retention, blurred vision, sedation, hypotension, arrhythmias, QT and QRS prolongation, hallucinations and sexual dysfunction Use with caution in people particularly at risk of adverse effects ie elderly, people with CV disease or epilepsy CI with monoamine oxidase inhibitors as serotonin levels can get too high

Answer 315

Diazepam | Lorazepam

Answer 316

First line treatment of seizures and status epilepticus Management of alcohol withdrawal reactions Short term treatment of severe anxiety or insomnia

Answer 317

Target GABA-a receptor which is a chloride channel that opens in response to binding GABA opening channel allows chloride to enter making cell more resistant to depolarisation Facilitate enhanced binding of GABA to GABA-a receptors and have widespread depressant effect on synaptic transmission Can thus cause, reduced anxiety, sleepiness, sedation, and anti-convulsion

Answer 318

Cause dose dependent drowsiness, sedation, coma and in overdose loss of airway reflexes which can lead to coma and death Use in elderly, those with respiratory or hepatic impairment and neuromuscular disease with care Increased sedative effects when used with other drugs such as alcohol, opioids With cytochrome P450 inhibitors may increase their effects

Answer 319

An anticonvulsant

Answer 320

First line treatment for epilepsy - specifically partial/focal seizures with/without secondary generalisation and for primary generalised seizures Trigeminal neuralgia to control pain and reduce attack severity

Answer 321

Incompletely understood - inhibits neuronal Na+ channels, stabilising resting membrane potential and reducing neuronal excitability May inhibit spread of seizure acitivty in epilepsy and control neuralgic pain by blocking synaptic transmission in trigeminal nucleus

Answer 322

GI disturbance, dizziness, ataxia, hypersensitivity skin rash, oedema, hyponatraemia CI in prior anti-epileptic hypersensitivity syndrome Used with caution in hepatic, renal and cardiac disease Reduces efficacy of drugs metabolised by P450 enzymes eg warfarin, oestrogens, progesterones Effects increased by cytochrome P450 inhibitors Efficacy reduced by drugs that lower seizure threshold eg SSRIs

Answer 323

Gabapentin | Pregabalin

Answer 324

Partial/focal epilepsies, usually as add on when other drugs such as carbamazepine insufficient Also used for neuropathic pain, mirgraine prophylaxis, and generalised anxiety disorder

Answer 325

Closely related to GABA Binds to voltage sensitive Ca2+ channels, where is prevents inflow of Ca2+ and thus inhibits neurotransmitter release - interfering with synaptic transmission and reducing neuronal excitability

Answer 326

Generally better tolerated Drowsiness, dizziness, ataxia Use with care in renal impairment Sedative effects enhanced when used with other sedating drugs

Answer 327

Parkinson's

Answer 328

Increases dopaminergic stimulation to basal ganglia Dopamine itself cannot cross BBB but levodopa as a dopamine precursor can Once in brain converted to dopamine in dopaminegic neurones

Answer 329

Nausea, drowsiness, confusion, hallucinations, hypertension Major issue - effects wear off towards end of dosage intervals Increasing dose can lead to excessive movement causing on/off effect Use with care in elderly and those with existing cognitive disease Use with caution in CVS disease Always give with decarboxylase inhibitor such as co-careldopa to reduce levodopas peripheral conversion before it is able to enter the brain - reduces nausea and lowers dose required Do not use with antipsychotics as they contraindicate effects of levodopa

Answer 330

Treating dyskinesia in Huntington's disease | Used as antipsychotic and antihypertensive

Answer 331

Monoamine neurotransmitters are dopamine, serotonin, noradrenaline and adrenaline Irreversibly blocks vesicular monoamine transporter which normally transports free intracellular noradrenaline, serotonin and dopamine for release across synapse Post synaptic cells not activated and symptoms decrease - effects long lasting until VMAT replenished

Answer 332

``` Nasal congestion GI disturbance Drowsiness/dizziness Hypotension and bradycardia so use with care in patients with CVS disease May also worsen asthma ```

Answer 333

Sumatriptan | Rizatriptan

Answer 334

Treatment of migraines and cluster headaches

Answer 335

Agonist of serotonin 5-HT-1b and 1d receptors in cranial blood vessels causing constriction and subsequent inhibition of pro-inflammatory neuropeptide release May also work on serotonin receptors in nerve endings to relieve pain through decrease in levels of substance P

Answer 336

Recurrence of migraine - more than without drug Rare risk of coronary spasm and cardiac events CI in previous/current severe CVD or stroke Use with caution in older people and FHx of stroke, CVD, diabetes and high cholesterol

Answer 337

Selegiline | Rasagiline

Answer 338

Parkinson's Alzheimer's Atypical depression

Answer 339

Inhibits activity of monoamine oxidase preventing breakdown of monoamine neurotransmitters (dopamine, serotonin, adrenaline, noradrenaline) and increasing their availability MAO-B preferentially targeted in Parkinson's and Alzheimer's disease as found to be increased

Answer 340

Hypertensive crisis if large amounts of tyramine are consumed so cut down on aged cheeses and alcohol Should not be used with other psychoactive drugs such as antidepressants and adrenaline

Answer 341

Rivastigmine | Donepezil

Answer 342

Alzheimer's Lewy body dementia Parkinson's Myasthenia gravis

Answer 343

Inhibit breakdown of acetylcholine by blocking site of acetylcholinesterase In neurodegenerative disorders used to treat memory and learning deficit symptoms which improve due to role of acetylcholine in cognition In myasthenia gravis too few acetylcholine receptors so with acetylcholinesterase blocked and acetylcholine transmission increased, then acetlycholine can bind to few receptors more easily and trigger more muscular contractions

Answer 344

Actions on parasympathetic nervous system can cause bradycardia, hypotension, hypersecretion, bronchoconstriction GI tract hypermotility Prolonged muscular contraction CI in urinary retention due to obstruction Use with care in people with CVS disease ie arrhythmias and in asthmatics