Neurology Flashcards

Question

What are the common causes of bacterial meningitis in infants?

Answer 1

Neisseria meningitidis Haemophilus influenzae Streptococcus pneumoniae

Answer 2

Neisseria meningitidis Streptococcus pneumoniae

Answer 3

Streptococcus pneumoniae Neisseria meningitidis Listeria monocytogenes

Answer 4

enteroviruses (e.g. coxsackievirus) herpes zoster virus varicella zoster virus

Answer 5

inflammation of the meninges

Answer 6

cryptococcus, histoplasma, blastomyces

Answer 7

extremes of age immunnocompromised non-vaccination crowding exposure to pathogens cranial anatomical defects cochlear implants sickle cell disease (due to impaired splenic function)

Answer 8

meningism (photophobia, neck stiffness, severe headache) fever altered consciousness seizures

Answer 9

non-blanching rash in children (meningococcal septicaemia) Kernig sign (can't extend knee when hip is flexed without pain) Brudzinski sign (when neck is flexed, knees + hips automatically flexed)

Answer 10

hypotonia poor feeding lethargy hypothermia bulging fontanelle

Answer 11

lumbar puncture + CSF analysis (sample taken from L3/4)

Answer 12

ceftriaxone/cefotaxime (3rd gen. cephalosporin) + steroids (dexamethasone)

Answer 13

none if enteroviral cause Aciclovir if cause is HSV or VZV

Answer 14

long course, high dose antifungals (e.g. fluconazole)

Answer 15

Increased opening pressure Cloudy yellow appearance Increased WCC (neutrophilia) Increased protein (>1g/L) Decreased glucose (<50% serum level)

Answer 16

Increased opening pressure Cloudy + fibrinous appearance Increased WCC (lymphocytosis) Increased protein (>1g/L) Decreased glucose (<50% serum level)

Answer 17

Normal opening pressure Clear, normal colour CSF Increased WCC (lymphocytosis) Normal protein levels Increased glucose (>60% serum level)

Answer 18

inflammation of the cerebral cortex

Answer 19

meningo-encephalitis

Answer 20

Herpes simplex varicella zoster parvoviruses HIV mumps measles

Answer 21

herpes simplex virus 1

Answer 22

immunocompromised extremes of age vaccination post-infection organ transplantation animal or insect bites location (e.g. increased risk of exposure to malaria, ebola, trypanosomiasis)

Answer 23

temporal lobe, presents with aphasia

Answer 24

fever headache focal neurology altered cognition/consciousness focal seizures rash lethargy and fatigue

Answer 25

lumbar puncture + CSF analysis (viral PCR testing) MRI head (GS) EEG recording swabs HIV testing

Answer 26

IV aciclovir if HSV encephalitis suspected

Answer 27

lasting fatigue and prolonged recovery change in mood/personality changes to memory and cognition chronic pain

Answer 28

a pus-filled pocket of infected material in the brain

Answer 29

fever headache changes to mental state focal neurological deficits grand mal seizures nausea vomiting neck stiffness

Answer 30

suddenly worsening headache, followed by emerging signs of meningism

Answer 31

acute neurological deficit lasting more than 24hrs of cerebrovascular cause

Answer 32

CT scan - abscess appears as a radiolucent space-occupying lesion

Answer 33

drain intracranial collection administer effective antibiotic therapy (early treatment is essential) eliminate primary source of infection

Answer 34

staph. aureus streptococus bacteriodes listeria spp.

Answer 35

fungi e.g. aspergillus, candida, cryptococcus protozoa e.g. toxoplasma gondii, entamoeba histolytica helminths e.g. taenia solium

Answer 36

Acute neurological deficit lasting more than 24hrs of cerebrovascular cause Divided into ischaemic (caused by vascular occlusion or stenosis) and haemorrhagic (caused by vascular rupture)

Answer 37

thrombus formation or embolus atherosclerosis shock vasculitis

Answer 38

trauma hypertension berry aneurysm rupture

Answer 39

CVD previous stroke or TIA atrial fibrillation carotid artery disease hypertension diabetes smoking vasculitis thrombophilia combined contraceptive pill over 55 years FHx

Answer 40

unilateral sudden onset of: weakness of limbs facial weakness onset dysphagia visual or sensory loss headache

Answer 41

F-face A - arm S - speech T - time (act fast and call 999)

Answer 42

Recognition Of Stroke In the Emergency Room

Answer 43

Loss of consciousness or syncope Seizure activity Asymmetric facial weakness Asymmetric arm weakness Asymmetric leg weakness Speech disturbance Visual field defect

Answer 44

Non-contrast CT head

Answer 45

hypoglycaemia hypertensive encephalopathy TIA

Answer 46

Aspirin 300mg STAT asap within 24hrs after ischaemic confirmed Thombolysis with alteplase (started asap within 4.5hrs of stroke symptom onset) Thrombectomy (offer asap and within 6 hrs of symptom onset)

Answer 47

IV mannitol for ↑ICP

Answer 48

clopidogrel 75mg OS atorvastatin 80mg carotid endarterectomy or stenting in patients with carotid artery disease

Answer 49

A tissue plasminogen activator which rapidly breaks down clots and can reserve stroke effects if given in time

Answer 50

Transient ischaemic stroke - an episode of neurological dysfunction caused by focal brain, spinal cord or retinal ischaemia without acute infarction where symptoms resolve within 24hrs.

Answer 51

2 or more strokes in one week, carries very high risk of developing into a stroke

Answer 52

carotid thrombo-emboli (29%) small-vessel occlusion (16%) in situ thrombosis of intracranial artery-to-artery embolism of thrombus as a result of stenosis or unstable atherosclerotic plaque (16%)

Answer 53

AF valvular disease carotid stenosis congestive heart failure hypertension diabetes mellitus smoking alcohol abuse advanced age

Answer 54

sudden onset and brief duration of symptoms (<24hrs) unilateral weakness of paralysis dysphagia ataxia, vertigo or loss of balance amaurosis fugax homonymous hemianopia diplopia

Answer 55

Often clinical diagnosis blood glucose, FBC, platelets, PT, INR, lipids, electrolytes, ECG

Answer 56

stroke hypoglycaemia seizure complex migraine

Answer 57

aspirin 300mg daily for 2 weeks then dual platelet therapy (aspirin and clopidogrel) for 3 weeks then clopidogrel lifelong as secondary prevention for CVD/stroke

Answer 58

- BP control - Antiplatelet agents (clopidogrel/aspirin) - Anticoagulants - stop smoking - statin for high cholesterol - reduce alcohol intake - lose weight - increase physical activity - healthy diet

Answer 59

rapidly developing signs of neurological dysfunction and/or headaches due to bleeding into the subarachnoid space

Answer 60

MC: berry aneurysm rupture in the circle of willis trauma

Answer 61

hypertension smoking family history Autosomal dominant polycystic kidney disease (ADPKD) alcohol /drug use Marfan Ehlers-danlos syndrome Pseudoxanthoma elasticum (connective tissue disorder) Neurofibromatosis type I

Answer 62

severe sudden onset headache Kernig sign (cant extend leg when knee is flexed) Brudzinski sign (knees automatically flex when neck is elevated) Depressed consciousness/loss of consciousness Nerve palsies CN III/VI (III - fixed dilated pupil, VI - non-specific signs of ↑ICP) neck stiffness and muscle aches eyelid, drooping, diplopia with mydriasis, orbital pain

Answer 63

CT head (star shape bleed) If CT head is indicative --> CT angiogram If CT head is unclear --> lumbar puncture (xanthochromia)

Answer 64

1st line = neurosurgery (endovascular coiling) + Nimodipine (CCB, ↓vasospasm + ↓BP)

Answer 65

caused by rupture of a bridging vein often due to deceleration injuries also seen in abused children (e.g. shaken baby syndrome)

Answer 66

trauma child abuse cortical atrophy (e.g. dementia) coagulopathy anticoagulant use advanced age (65+)

Answer 67

typically result from torsional or shear forces causing disruption of bridging cortical veins emptying into dural venous sinuses

Answer 68

gradual onset with latent period --> small amount of bleeding which accumulates over time + autolysis of blood --> symptoms after days/weeks/months

Answer 69

nausea/vomiting headache diminished eye/verbal/motor responses confusion

Answer 70

NCCT head (sickle-shaped haematuria)

Answer 71

sugery: burr hole + craniotomy IV mannitol to ↓ICP

Answer 72

an acute haemorrhage between the dura mater and inner surface of the skull

Answer 73

most commonly caused by skull trauma in the temporoparietal region, typically following a fall, assault or sporting injury can also occur secondary to vein rupture, arteriovenous abnormalities or bleeding disorders

Answer 74

head trauma age 20-30yrs

Answer 75

reduced GCS (with lucid interval intially) headaches vomiting confusion seizures pupil dilation

Answer 76

NCCT (egg shaped haematoma - due to blood being contained by dura and skull)

Answer 77

Urgent surgery (craniotomy + vessel ligation) IV mannitol to ↓ICP

Answer 78

epilepsy carotid dissection carbon monoxide poisoning subdural haematoma subarachnoid haemorrhage

Answer 79

also known as retinal transient ischaemic attack = a sudden, short-term, painless loss of vision in one eye

Answer 80

stenosis or occlusion of internal carotid artery or central retinal artery inflammation of optic nerve or nervous system giant cell arteritis in individuals >60yrs old

Answer 81

chronic and progressive neurological disorder caused by demyelination of the myelinated neurons in the CNS

Answer 82

Relapsing-remitting = symptoms then incomplete recovery then symptoms return Primary progressive = gradual deterioration without recovery Secondary progressive = relapsing remitting --> primary progressive (around 75% of RR cases evolve to this)

Answer 83

female 20-40yrs autoimmune disease FHx EBV vitamin D deficiency

Answer 84

Inflammation around the myelin covering nerves in the CNS and infiltration of immune cells causes damage to the myelin and affects the way the electrical signals travel along the nerves

Answer 85

optic neuritis (mc) eye movement abnormalities (double vision, internuclear ophthalmoplegia, conjugate lateral gaze disorder) focal weakness (Bell's palsy, Horner's syndrome, limb paralysis, incontinence) focal sensory symptoms (trigeminal neuralgia, numbness, paraesthesia, Lhermitte's sign) ataxia (sensory or cerebellar)

Answer 86

McDonald criteria (2 attacks disseminated in time (separate events) + space (different parts of CNS affected) MRI scan (GS)

Answer 87

acutely (during symptomatic episodes) --> IV methylprednisolone patient education prophylaxis --> B interferon (DMARDs, biologic therapies)

Answer 88

migraine with aura hypoglycaemia hypothyroidism electrolyte abnormalities

Answer 89

More common in women 20-40 most common age for diagnosis More common in white More common in northern latitudes Symptoms will improve in pregnancy and post-partum period

Answer 90

worsening of MS symptoms following a rise in temperature, such as a hot bath

Answer 91

demyelination of the optic nerve which presents with: - unilateral reduced vision - central scotoma - pain on eye movement - impaired colour vision (red)

Answer 92

2 or more relapses and either: - objective evidence of two or more lesions - objective evidence of one and a reasonable history of a previous relapse 'objective evidence' = abnormality on neurological exam, MRI or visual evoked potentials

Answer 93

oral or IV prednisolone plasma exchange: to remove disease-causing antibodies

Answer 94

flare ups - IV methylprednisolone DMARDs - ocrelizumab Beta-interferon - decreases the level of inflammatory cytokines Monoclonal antibodies Glatiramer acetate (immunomodulator) Fingolimod

Answer 95

either hemisphere: hemiparesis hemisensory loss visual field defect dominant hemisphere (usually left) language dysfunction - expressive dysphasia - receptive dysphasia - dyslexia - dysgraphia (inability to write) non-dominant hemisphere anosognosia (impaired ability to comprehend illness) - neglect of paralysed limb - denial of weakness visuospatial dysfunction - geographical agnosia - dressing apraxia - contructional apraxia

Answer 96

- unsteadiness - visual disturbance - slurred speech - headache - vomiting - others e.g. memory loss, confusion

Answer 97

Ischaemic - 80% Haemorrhagic - 20%

Answer 98

large vessel disease (50%) small vessel disease (25%) cardioembolic (20%) cryptogenic/rarities (5%)

Answer 99

primary intracerebral haemorrhage subarachnoid haemorrhage

Answer 100

epileptic seizure space occupying lesion (subdural, tumour, arteriovenous malformation) infection metabolic (e.g. hyponatraemia/hypoglycaemia/alcohol/drugs) multiple sclerosis functional neurological disorder (FND) migraine

Answer 101

1) large-artery atherosclerosis 2) cardioembolism 3) small-vessel occlusion 4) stroke of other determined etiology 5) stroke of undetermined etiology

Answer 102

carotid or vertebral dissection

Answer 103

leakage of blood directly into brain tissue due to : - hypertension (weakens deep perforating blood vessels) - amyloidosis - arteriovenous malformation - aneurysm rupture

Answer 104

trauma warfarin bleeding into a tumour Not classed as strokes but can cause similar symptoms

Answer 105

High grade glioma (85% of all new cases of malignant primary brain tumour)

Answer 106

headache + features of raised ICP and/or focal neurology new onset focal seizure rapidly progressive focal neurology past history of other cancer

Answer 107

a grade IV glioma, which is a fast-growing and aggressive brain tumour

Answer 108

multifocal - can be seen to have multiple areas of high grade cancerous formations joined together by other abnormal brain tissue (2-20% of all glioblastomas) multicentric - more than one GBM tumour that has arisen in the brain at the same time, or within a very short timeframe which have normal brain tissue between them

Answer 109

abnormal growth originating from cells within the brain (gliomas, germ cell tumours, meninigiomas)

Answer 110

lungs breast colorectal testicular renal cell malignant melanoma

Answer 111

majority no cause found ionising radiation 5% family history (associated genetic syndromes (neurofibromatosis, tuberose sclerosis, Von Hippel-Lindau disease) immunosuppression

Answer 112

Wide variation depending on tumour type, grade and site Headache (woken by headache, worse in the morning, associated with N/V, exacerbated by coughing, sneezing, drowsiness) Seizures Focal neurological symptoms (symptoms specific to site in the brain e.g. loss of right arm motor function due to damage to left side motor cortex) - hemiparesis, hemisensory loss, visual field defect, dysphasia Other non-focal symptoms (personality change/behaviour, memory disturbance, confusion) Signs of ↑ICP - altered mental state, visual field defects, seizures, unilateral ptosis, 3rd and 6th nerve palsies, papilloedema (on fundoscopy)

Answer 113

low grade - typically present with seizures (can be incidental finding) high grade - rapidly progressive neurological deficit + symptoms of raised intracranial pressure

Answer 114

1st line - contrast CT GS - MRI other - functional MRI (shows which areas of the brain are most active)

Answer 115

Steroids - reduce oedema Palliative care Chemotherapy - temozolamide, PCV (procarbazine, lomustine + vincristine) Radiotherapy - mainstay, radical vs palliative Surgery - biopsy or resection

Answer 116

Surgery - early resection Radiotherapy and early chemotherapy

Answer 117

1 - slow growing, non-malignant, and associated with long-term survival 2 - have cytological atypia. These tumours are slow growing but recur as higher-grade tumours 3 - have anaplasia and mitotic activity. These tumours are malignant 4 - anaplasia, mitotic activity with microvascular proliferation, and/or necrosis. These tumours reproduce rapidly and are very aggressive malignant tumours.

Answer 118

increases the activity of GABA which has a relaxant affect on the brain by stopping the release of excitatory neurotransmitters

Answer 119

medical emergency defined as seizures lasting more than 5 minute or >= 2 seizures within a 5-minute period without the person returning to normal between them

Answer 120

ABCDE approach: - securing the airway - giving high concentration O2 - checking blood glucose levels - gaining IV access Medical treatment: - benzodiazepine 1st line, repeated after 5-10 mins if the seizure continues - 2nd line options (following 2x benzodiazepine) are IV levetiracetam, phenytoin or sodium valproate - 3rd line options are phenobarbital or general anaesthesia

Answer 121

an umbrella term for chronic conditions where patients have a tendency to have recurrent, unprovoked epileptic seizures

Answer 122

Transient episodes of abnormal electrical in the brain which cause changes in behaviour, sensation or cognitive processes

Answer 123

Myoclonic jerks Absence Primary generalised tonic clonic

Answer 124

also known as a partial seizure, these occur in an isolated brain area and affect hearing, speech, memory and emotions - patients remain awake during simple focal seizures (focal aware seizure) but lose awareness during complex focal seizures (focal impaired awareness seizure)

Answer 125

these depend on the location of the abnormal activity: - deja vu - strange smells, tastes, sight or sound sensations - unusual emotions - abnormal behaviours

Answer 126

the frontal lobe

Answer 127

the parietal lobe

Answer 128

tonic-clonic, absence, myoclonic, tonic, atonic

Answer 129

FHx CNS infection history Head trauma Prior seizure events/suspected seizure events Hx of substance use Premature birth Multiple or complicated febrile seizures

Answer 130

prodrome = mood changes, days before aura = minutes before, deja vu + automatisms (lip smacking, rapid blinking) - not always present (most commonly seen in temporal lobe epilepsy) ictal event = seizure post-ictal period = symptoms such as headache, confusion, ↓GCS, Todd's paralysis, dysphasia, amnesia, sore tongue (pts bite tongue during ictal phase)

Answer 131

loss of awareness memory lapse feeling confused difficulty hearing odd smells, sounds or tastes loss of muscle control changes in speech/ability to speak

Answer 132

confusion amnesia drowsiness hypertension headache nausea

Answer 133

can occur from sleep can be associated with other brain dysfunction lateral tongue bite deja vu incontinence

Answer 134

EEG, ECG, CT head + MRI

Answer 135

1 of: - 2+ unprovoked seizures occurring more than 24hrs apart - 1 unprovoked seizure and a probability of future seizures (considered >60% risk in 10yrs) - Diagnosis of an epileptic syndrome

Answer 136

aim is to be seizure free on the minimum anti-epileptic medications 1st line = sodium valproate also lamotrigine (sv is teratogenic) ideally pts should be on monotherapy with a single anti-epileptic drug

Answer 137

no aura loss of consciousness tonic (muscle tensing, fall to floor) and clonic (muscle jerking) episodes typically tonic before clonic eyes open and upward gazing incontinence tongue biting post-ictal period

Answer 138

1st line: sodium valproate 2nd line: lamotrigine or carbamazepine

Answer 139

typically occur in children patient becomes blank, stares into space and then abruptly returns to normal last 10-20 seconds

Answer 140

sudden brief muscle contractions like a sudden jump patient normally remains awake during the episode occur in various forms of epilepsy but typically happen in children as part of juvenile myoclonic epilepsy

Answer 141

Jacksonian march + Todd's palsy

Answer 142

aura, dysphagia, post-ictal period

Answer 143

vision changes

Answer 144

1st: carbamazepine or lamotrigine 2nd: sodium valproate or levetiracetam

Answer 145

simple: no LOC, patient awake + aware, uncontrollable muscle jerking confined to one part of body complex: LOC, patient unaware, post-ictal period

Answer 146

Vascular Infection Trauma Autoimmune e.g. SLE Metabolic e,g. Hypocalcaemia Idiopathic e.g. epilepsy Neoplasms Dementia + Drugs (cocaine) Eclampsia

Answer 147

non-epileptic seizures which present with ictal symptoms as a result of mental processes triggered by internal or external aversive stimuli

Answer 148

situational duration 1-20 mins dramatic motor phenomena/prolonged atonia eyes closed ictal crying and speaking suprisingly rapid or slow post-ictal recovery history of psychiatric illlness, other somatoform disorders

Answer 149

transient loss of consciousness due to cerebral hypoperfusion, characterised by a rapid onset, short duration, and spontaneous compete recovery

Answer 150

sweating, nausea, pallor, prolonged standing position, hyperventilation, increased heart rate

Answer 151

neurally mediated/reflex syncope orthostatic hypotension cardiac arrhythmias structural cardiac or cardiopulmonary disease cerebrovascular substance abuse, alcohol intoxication psychogenic

Answer 152

most patients with neurally mediated syncope (NMS) just need reassurance and education about how to avoid recurrence if syncope is very frequent, unpredictable or could occur during high risk activities like driving treatments like tilt-training, isometric counterpressure manoeuvres can help for syncope with a clear cause this should be treated

Answer 153

a rhythmic oscillatory movement of a body part, resulting from the contraction of opposing muscle groups

Answer 154

fine tremor (low amplitude) symmetrical more prominent with voluntary movement worse when tired, stressed or after caffeine improved by alcohol absent during sleep

Answer 155

Parkinson's disease Multiple sclerosis Huntington's chorea Hyperthyroidism Fever Dopamine antagonists (e.g. antipsychotics)

Answer 156

There is no definitive treatment If not causing functional or psychological problems it does not require treatment Medications which may improve symptoms are: - Propanol (non-selective beta-blocker) - Primidone (barbiturate anti-epileptic)

Answer 157

progressive reduction of dopamine in the basal ganglia of the brain, leading to disorders of movement

Answer 158

FHx increased age male

Answer 159

resting tremor, rigidity, bradykinesia

Answer 160

“pill rolling tremor”, asymmetrical, 4-6hz, worse at rest, improves with intentional movement

Answer 161

“cogwheel”, when limb is passively flexed and extended tension in the arm will be felt which gives way to movement in small increments

Answer 162

Depression Sleep disturbance and insomnia Loss of the sense of smell (anosmia) Postural instability Cognitive impairment and memory problems

Answer 163

clinical diagnosis based on symptoms and examination DaTSCAN (shows whether there is a loss of dopaminergic neurons in the striatum)

Answer 164

Individual specific depending on symptoms, response to medications No cure Levodopa (synthetic dopamine) combined with peripheral decarboxylase inhibitors (stop levodopa being broken down before it reaches the brain) => co-benyldopa (levodopa + benserazide), co-careldopa (levodopa + carbidopa) COMT inhibitors - entacapone (metabolises levodopa in the body and brain, taken with levodopa + decarboxylase inhibitor) Dopamine agonists - mimic dopamine in the basal ganglia and stimulate dopamine receptors - bromocriptine, pergolide, cabergoline Monoamine oxidase-B inhibitors

Answer 165

dyskinesia (abnormal movements associated with excessive motor activity) e.g. - dystonia (excessive muscle contraction leading to abnormal postures or exaggerated movements) - chorea (abnormal jerking/random movements) - athetosis (involuntary twisting or writhing movements, usually in the fingers, hands or feet)

Answer 166

Neurodegenerative disease which causes upper and lower motor neuron signs

Answer 167

amyotrophic lateral sclerosis - most common progressive bulbar palsy progressive muscular atrophy primary lateral sclerosis

Answer 168

FHx Smoking Exposure to heavy metals and certain pesticides Age

Answer 169

gradual progressive weakness of the muscles throughout the body (particularly affecting the limbs, trunk, face and speech) Fatigue when exercising Clumsiness Dropping things more often Dysarthria (slurred speech) Signs of LMN disease - muscle wasting, hypotonia, fasciculations, hyporeflexia Signs of UMN: hypertonia, spasticity, hyperreflexia, plantar responses

Answer 170

muscle wasting hypotonia fasciculations hyporeflexia

Answer 171

hypertonia spasticity hyperreflexia plantar responses

Answer 172

mainly clinical EMG (shows fibrillation potentials due to degeneration of muscle with LMN dysfunction)

Answer 173

No cure Riluzole (antiglutaminergic) - slows progression of disease and can extend survival by a few months in ALS Non-invasive ventilation (breathing support at night) Supportive - physiotherapy, breathing support if necessary

Answer 174

respiratory failure, aspiration pneumonia, swallowing failure

Answer 175

acute paralytic polyneuropathy affecting the peripheral nervous system

Answer 176

campylobacter jejuni + viruses; CMV, EBV, HSV

Answer 177

undercooked poultry (risk of C. jejuni) influenza, CMV , EBV, Zika, Hep A,B,C,E surgery trauma hodgkin's lymphoma mycoplasma pneumonia

Answer 178

molecular mimicry - organisms produce antigens very similar to those on schwann cells results in antibody production against schwann cell --> demyelination + acute polyneuropathy

Answer 179

Ascending symmetrical muscle weakness (+paralysis) Loss of deep tendon reflexes Loss of sensation in the peripheries or neuropathic pain Autonomic involvement in around 50% Respiratory failure in 35% → must always monitor GB patients breathing

Answer 180

Bilateral and flaccid limb weakness Decreased or absent deep tendon reflexes in weak limbs Monophasic course and time between onset-nadir 12-28 days CSF cell count <50/ul CSF protein concentration > normal NCS findings consistent with one of the subtypes of GBS Absence of alternative diagnosis for weakness The criteria are marked from 1-4 levels of diagnostic certainty

Answer 181

Diagnosis is made using the Brighton criteria supported by investigations: - nerve conduction studies (showing reduced signal through the nerves) - lumbar puncture at L3/4 --> raised protein + normal WCC (=inflammation but no infection)

Answer 182

IV Ig for 5 days (1st line) Plasmapheresis Supportive care Venous thromboembolism prophylaxis Severe case + resp failure --> need intubation, ventilation and ITU admission

Answer 183

neurological emergency resulting from thiamine deficiency with varied neurocognitive manifestations typically involving mental status changes and gait and oculomotor dysfunction

Answer 184

alcohol dependence AIDS cancer and treatment with chemotherapeutic agents malnutrition Hx of GI surgery

Answer 185

Acute or subacute thiamine deficiency in a susceptible person. Thiamine deficiency leads to decreased activity of thiamine-dependent enzymes which triggers a sequence of metabolic events resulting in energy compromise and ultimately neuronal death. The areas commonly affected include the medial dorsal thalamic nucleus, mammillary bodies, the periaqueductal grey matter, and the floor of the fourth ventricle.

Answer 186

Ataxia Confusion Mental slowing, impaired concentration, and apathy Classic triad: ophthalmoplegia, mental status changes, gait dysfunction (present in only 10% patients)

Answer 187

FBC (macrocytic anaemia), LFTS (deranged) Clinically diagnosed

Answer 188

high dose parenteral thiamine for 5 days acutely + magnesium sulphate + multivitamins oral thiamine prophylactically

Answer 189

when Wernicke's left too long without treatment --> severe thiamine deficiency

Answer 190

describes the spectrum of disease resulting from thiamine deficiency

Answer 191

most common and rapidly progressive type of muscular dystrophy (progressive generalised muscle disease) caused by the absence of dystrophin on the X-chromosome

Answer 192

X-linked recessive mutated dystrophin gene

Answer 193

Dystrophin is a cytoskeletal protein providing structural stability to the dystroglycan complex in cell membranes, most significantly in skeletal muscle. The absence of dystrophin results in ongoing cell membrane depolarisation due to calcium entering the cell which causes ongoing degeneration and regeneration of muscle fibres. Degeneration is faster than regeneration, and muscle fibres undergo necrosis. Muscle proteins are replaced by adipose and connective tissue, causing progressive muscle weakening.

Answer 194

Imbalance of lower limb strength Lower extremity musculotendinous contractures Delayed motor milestones Calf hypertrophy Ambulation difficulty and falls Diminished muscle tone and deep tendon reflexes Normal sensation

Answer 195

Specific technique to stand up from a lying position where the person uses their hands and arms to 'walk' up their own body from a squatting position due to lack of thigh and hip muscle strength.

Answer 196

serum creatine kinase genetic testing clinical presentation electromyogram muscle biopsy

Answer 197

Becker muscular dystrophy Limb-gordle muscular dystrophies Emery-dreifuss muscular dystrophies Polymyositis

Answer 198

No curative treatment Oral steroids to slow muscle weakness progression Creatine supplements occupational therapy, physio, medical appliances surgical and medical management of complications (e.g. spinal scoliosis, heart failure)

Answer 199

rare neurological condition characterised by a lesion in the spinal cord which results in weakness or paralysis on one side of the body and a loss of sensation on the opposite side

Answer 200

traumatic injury to spine or neck other spinal disorders (cervical spondylosis, arachnoid cyst, epidural haematoma) bacterial/viral infection (meningitis, myelitis, herpes, tuberculosis) radiation exposure MS

Answer 201

caused by lateral hemi-section of the spinal cord severing the pyramidal tract (already crossed in the medulla), the uncrossed dorsal columns and the crossed spinothalamic tract

Answer 202

Ipsilateral loss of all sensory modalities at level of lesion Ipsilateral flaccid paralysis at the level of the lesion Ipsilateral loss of position sense and vibration below the lesion Contralateral loss of pain/temperature sensation below the lesion Ipsilateral motor loss below the level of the lesion

Answer 203

MRI (GS) Myelogram + CT, blood tests, lumbar puncture

Answer 204

MND Progressive spinal muscular atrophy Primary lateral sclerosis Stroke

Answer 205

Most individuals with this syndrome will recover majority of function No specific treatment, will usually focus on underlying cause Occupational therapy, physiotherapy, medical appliances High dose steroids (methylprednisolone) Surgery Analgesia

Answer 206

low bp spinal shock depression abdominal enlargement lung/UT infections PE paralysis

Answer 207

inherited disease affecting the peripheral motor and sensory neurones - also known as hereditary motor and sensory neuropathy - there are various types with different genetic mutations and pathophysiology

Answer 208

autodominant mutation on chromosome 17;PUP 22 gene

Answer 209

A- alcohol B- B12 deficiency C- cancer and CKD D- diabetes + drugs E - every vasculitis

Answer 210

Foot drop (common peroneal palsy) Stork legs (very thin calves) Hammer toes (curled up toes) Pes cavus → high arched feet ↓Deep tendon reflexes Awkward or unusually high gait Frequent tripping or falling Decreased sensation or a loss of feeling in legs and feet

Answer 211

Clinical evaluation EEGs, motor conduction velocities, DNA bloods

Answer 212

No cure Supportive treatment e.g. analgesia for neuropathic pain Orthotics Physiotherapy Surgical treatment (for severe joint deformities)

Answer 213

motor neuropathy sensory neuropathy autonomic nerve neuropathy combination neuropathies

Answer 214

demyelination (Guillain-Barre, B-12 deficiency) T2DM surgery pathology e.g. infection, endocrine, RA

Answer 215

demyelination axonal damage nerve compression vasanervosum infarction wallerian degeneration - nerve cut and distally die

Answer 216

Muscle weakness Cramps Muscle twitching Loss of muscle and bone Changes in skin, hair or nails Numbness Loss of sensation or feeling in body parts Loss of balance or other functions as a side effect of the loss of feeling in the legs, arms or other body parts Emotional/sleep disturbances Loss of bladder control

Answer 217

bloods, spinal fluid tests, muscle strength tests, vibration detection tests GS: CT/MRI electromyography and nerve conduction studies nerve and skin biopsy

Answer 218

treat underlying condition (e.g. diabetes) analgesia

Answer 219

describes a clinical presentation of progressive motor and sensory deficits in the distribution of specific peripheral nerves

Answer 220

Wegeners AIDS/amyloidosis RA DMT2 Sarcoidosis Polyarteritis nodosa Leprosy Carcinomas

Answer 221

numbness tingling abnormal sensation burning pain paralysis lack of controlled movement of a body part

Answer 222

symptoms caused by pressure on median nerve as it passes through the carpal tunnel

Answer 223

Female Hypothyroidism Acromegaly Pregnancy RA Obesity Diabetes Perimenopause Repetitive strain

Answer 224

Compression is the result of either swelling of the tunnel contents (e.g. tendon sheath inflammation due to repetitive strain) or narrowing of the tunnel The median nerve provides sensation to the palm and motor function to the thenar muscle responsible for thumb movements.

Answer 225

gradual onset - weakness of grip + aching hand/forearm (worse at night and relieved by hanging hand over side of bed, wake + shake) - paraesthesia of hand - burning sensation - wasting of thenar eminence

Answer 226

flex fist at wrist for 1 minute --> positive = paraesthesia + pain

Answer 227

tapping wrist causes tingling

Answer 228

EMG (electromyography)

Answer 229

Wrist splint at night + steroid injection (acutely very painful) Last resort = surgical decompression

Answer 230

nerve (roots C5-T1) Radial nerve mostly innervates extensor arm muscle so lesion causes weakness of extensor muscle --> wrist drop

Answer 231

accuracy and coordination motor control and learning helps with timing and sensory acquisition helps prediction of the sensory consequences of action eye movements, speech, limb movements, fine motor skills, gait, posture, balance, cognition

Answer 232

'lack of order' describes heterogenous group of disorders affecting balance, coordination and speech

Answer 233

inherited: autosomal dominant (SCA6, EA2) and recessive (Friedrich's ataxia, SPG7) acquired: toxic/metabolic (alcohol, vitamin defs, drugs), immune mediated (paraneoplastic cerebellar degeneration, gluten related), infective (post-infectious), degenerative (multi-system atrophy cerebellar variant), structural (trauma, neoplastic)

Answer 234

Genetic, progressive, neurodegenerative movement disorder which typically presents at age 10-15 years old

Answer 235

dizzy - unsteady/wobbly/clumsy falls, stumbles difficulty focusing/double vision/ 'oscillopsia' (blurred, jumpy vision) slurred speech problems with swallowing tremor problems with dexterity /fine motor skills

Answer 236

- nystagmus/jerky (saccadic) pursuit/hypo or hypermetropic saccades/optic atrophy/ptosis dysarthria - intention tremor/myoclonus - dysmetria/past pointing/dysdiadochokinaesia (difficulty performing quick/alternating movements) - heel - shin ataxia - gait/limb/truncal ataxia - decreased tone/reflexes

Answer 237

mild - mobilising independently or with one walking aid moderate - mobilising with 2 walking aids or walking frame severe - predominantly wheelchair dependent

Answer 238

* FBC, U&E, extended LFT’s * HbA1c, B12, folate, TSH * ESR, CRP * gluten related serology* (can only be requested in sheffield)

Answer 239

to demonstrate cerebellar atrophy and/or dysfunction to exclude cerebrovascular damage, primary tumours, hydrocephalus, demyelinating disorders, white matter disease, cerebellar dysgenesis/malformations

Answer 240

Criteria which differentiate the types of ischaemic stroke according to the circulation affected

Answer 241

TACS, PACS, POCS, Lacunar stroke

Answer 242

- Unilateral weakness and/or sensory deficit of the face, arm and leg - Homonymous hemianopia - Higher cerebral dysfunction (dysphasia, visuospatial disorder)

Answer 243

total anterior circulation stroke, which affects the areas of the cortex supplied by both the middle and anterior cerebral arteries

Answer 244

posterior anterior circulation stroke = less severe form of TACS where only part of the anterior circulation has been compromised

Answer 245

Two of the following: Unilateral weakness (and/or sensory deficit) of the face, arm and leg Homonymous hemianopia Higher cerebral dysfunction (dysphasia, visuospatial disorder)

Answer 246

posterior circulation stroke = damage to the area of the brain supplied by the posterior circulation (e.g. cerebellum and brainstem)

Answer 247

One of the following: - cranial nerve palsy and a contralateral motor/sensory deficit - bilateral motor/sensory deficit - conjugate eye movement disorder cerebellar dysfunction (e.g. vertigo, nystagmus, ataxia) - isolated homonymous hemianopia

Answer 248

subcortical stroke which occurs secondary to small vessel disease no loss of higher cerebral functions

Answer 249

pure sensory stroke pure motor stroke sensori-motor ataxic hemiparesis

Answer 250

glove and stocking loss of sensation

Answer 251

30% unknown endocrine- DM, hypothyroidism inflammatory - Guillain-Barre, CIDP, SLE infective - lyme disease, HIV nutritional - Vitamin B12 def, B6 toxicity metabolic - porphyria, copper def genetic - CMT disease, Friedrich's ataxia neoplastic and paraneoplastic - MGUS, SSCA drugs - vincristine, phenytoin, amiodarone

Answer 252

ulnar nerve treatment = splint , simple analgesia

Answer 253

peroneal nerve palsy treatment = physiotherapy, splint/brace + analgesia

Answer 254

progressive muscle weakness which is a result of autoimmune attack directed against the voltage-gated calcium channels on the presynaptic membrane

Answer 255

typically occurs in patients with SCLC and is a result of antibodies produced by the immune system against voltage-gated calcium channels in SCLC cells these antibodies also target and damage voltage-gated calcium channels on the presynaptic motor nerve terminal resulting in a loss of functional voltage gated calcium channels at the motor nerve terminals

Answer 256

- proximal leg muscle weakness - affects intraocular muscle causing diplopia, levator muscles causing ptosis, oropharyngeal muscle causing - slurred speech and dysphagia - dry mouth, blurred vision, impotence, dizziness due to autonomic dysfunction - reduced DTRs

Answer 257

when reflexes can become temporarily normal following period of strong muscle contraction

Answer 258

FBC, serology, CT or MRI Repetitive nerve stimulation studies Electromyography

Answer 259

Acute/chronic inflammatory demyelinating polyradiculopathy Dermatomyositis Multiple sclerosis

Answer 260

Amifampridine (blocks voltage gated K+ channels in the presynaptic cells) Immunosuppressants (prednisolone/azathioprine) IV immunoglobulins Plasmapheresis

Answer 261

an autoimmune condition that causes muscle weakness which progressively worsens with exercise and improves on rest

Answer 262

In around 85% of patients with MG, acetylcholine receptor antibodies are produced by the immune system which bind to postsynaptic neuromuscular junction receptors and prevents acetylcholine from stimulating the receptor and triggering muscle contraction. As the receptors are used more during muscle activity, more of them become blocked up and so muscle weakness increases with use. The antibodies also activate the complement system leading to damage to cells at the postsynaptic membrane which worsens symptoms.

Answer 263

Extraocular muscle weakness causing double vision (diplopia) Eyelid weakness causing drooping of the eyelids (ptosis) Weakness in facial movements Difficulty with swallowing Fatigue in the jaw when chewing Slurred speech Progressive weakness with repetitive movements

Answer 264

FVC, muscle fatigability testing (repeated blinking → ptosis, prolonged upward gazing → diplopia) Serology (ACH-R, MuSK, LRP4 antibodies) CT/MRI, edrophonium test (blocks enzymes and stops breakdown of ACh → temporarily increased ACh and relieved muscle weakness)

Answer 265

Reversible ACh inhibitors (pyridostigmine or neostigmine) Immunosuppression (prednisolone or azathioprine) Thymectomy Monoclonal antibodies (rituximab, ecluzimab)

Answer 266

acute worsening of symptoms which can lead to resp failure

Answer 267

IV immunoglobulins and plasmapheresis

Answer 268

autosomal dominant genetic condition that causes a progressive deterioration in the nervous system

Answer 269

trinucleotide repeat disorder involving the HTT on chromosome 4 <35 repeats --> normal 35-55 --> huntington's 60+ --> severe huntington's

Answer 270

genetic anticipation which is where successive generations have more repeats resulting in earlier age of onset and increased severity of disease

Answer 271

Typically begins with cognitive, psychiatric or mood problems (e.g. depression) Chorea (excessive limb jerking) Eye movement disorders Dysarthria Dysphagia Dementia Motor impersistence (can sustain movement)

Answer 272

no treatment options to slow or stop the progression of the disease aim of management is to support and maintain quality of life and relieve symptoms medical: antipsychotics (olanzapine), benzodiazepines (diazepam), dopamine-depleting agents (tetrabenazine), antidepressants speech and language therapy genetic couselling palliative care

Answer 273

15-20 years after symptom onset

Answer 274

the most common form of dementia which progressively destroys memory and cognitive ability

Answer 275

dementia resulting from cerebrovascular damage and stroke

Answer 276

Multi-infarct dementia → series of small strokes which together cause symptoms Subcortical dementia → small penetrating arteries affected (small vessel damage) Stroke-related dementia → 3-% of ischaemic strokes lead to this

Answer 277

Vascular: smoking, diabetes, AF< dyslipidemia, hypertension, age Age Genetics FHx (10-30% increased risk with affected 1st degree relative) Trisomy 21 (early onset dementia) Gender - more common in women Cognitive reserve (social isolation, left education early

Answer 278

increased quantities of B-amyloid mostly in hippocampus, parietal and temporal lobes causes damage to brain tissue

Answer 279

reduced blood flow to neurons leading to ischemia and cell death

Answer 280

spherical intracellular deposits formed from a-synuclein + ubiquitin

Answer 281

caused by mutations in TDP43 (DNA binding protein) or TAU protein (microtubule protein)

Answer 282

short term memory loss, difficulty finding words, poor insight, disorientation

Answer 283

stepwise deterioration, impaired planning, organising, and judgements which present early

Answer 284

fluctuating cognition, visual hallucinations, parkinsonian features (e.g. bradykinesia, cogwheel rigidity, falls risk, autonomic dysregulation)

Answer 285

Behavioural variant (most common) - personality/behaviour changes early on, disinhibition/social withdrawal, pick bodies in cytoplasm Semantic variant - language difficulties - finding words, comprehension, fluent aphasia Non-fluent variant - progressive non-fluent speech

Answer 286

clinical history + physical exam, MMSE brain biopsy (GS) bloods, CT head, genetic testing

Answer 287

Conservative, risk reduction, slow progression ; social stimulation, exercise No cure For Alzheimer’s = Acetylcholinesterase-inhibitors (Donepezil/Rivastigmine) Vascular = hypertensives e.g. ramipril

Answer 288

unilateral periorbital pain with autonomic features (15-180 mins duration)

Answer 289

Male Smoking Genetics

Answer 290

Crescendo unilateral periorbital excruciating pain, may affect temples too Autonomic features of face flushing Conjunctival infection + lacrimation Ptosis Miosis Rhinorrhoea (running nose)

Answer 291

5 ≤ similar attack

Answer 292

Acute = triptans (sumatriptan) Prophylaxis = verapamil (CCB)

Answer 293

bilateral generalised headaches which radiate to neck

Answer 294

Stress Sleep deprivation Bad posture eyestrain Depression Alcohol Skipping meals dehydration

Answer 295

Rubber band, tight around head, bilateral pain, also feel it in trapezius mild -moderate severity No motion sickness, photophobia, aura

Answer 296

simple analgesia

Answer 297

Unilateral pain in 1≤ trigeminal branches (90%) 10% are bilateral

Answer 298

eating, shaving, talking, brushing teeth, cold weather, spicy food, caffeine and citrus fruits

Answer 299

MS (20x more likely) Increased age Female

Answer 300

electric shock pain lasting up to 2 mins

Answer 301

Treatment = carbamazepine (anti-convulsant) Consider surgery if no other treatment effective (decompression or intentional damage to trigeminal nerve e.g. stereotactic radiotherapy)

Answer 302

surgical emergency caused by compression of the nerve roots of the cauda equina

Answer 303

Compression can be caused by: Herniated disc Tumours Spondylolisthesis Abscess Trauma

Answer 304

Lumbar disc herniation Spinal trauma Spinal surgery spinal epidural abscess Anticoagulation therapy Spinal stenosis Spinal tumour Under 50yrs old

Answer 305

Bladder dysfunction Lower limb weakness Saddle paraesthesia/anaesthesia Bowel dysfunction Lower back pain Sciatica Sexual dysfunction

Answer 306

Spinal MRI + testing nerve roots/reflexes

Answer 307

Emergency decompression surgery to prevent permanent neurological dysfunction

Answer 308

saddle anaesthesia, loss of sensation in bladder or rectum, urinary retention or incontinence, faecal incontinence, bilateral sciatica, bilateral or severe motor weakness in the legs , reduced anal tone on PR examination

Answer 309

compression of C1-L1/2

Answer 310

Cancer + metastases ≥40 years old Immune system disorders Radiation Genotype features

Answer 311

progressive leg weakness with limbs signs (e.g. contralateral hyperreflexia, Babinski +ve, spasticity) back pain sensory loss below lesion sphincter involvement uncommon (late = v bad sign)

Answer 312

MRI, CXR if malignancy suspected

Answer 313

neurosurgery - laminectomy, microdisectomy

Answer 314

L5/S1 lesion due to spinal; IV disc herniation/prolapse non-spinal; piriformis syndrome, tumours, pregnancy

Answer 315

the pain radiates through the buttock and back of one leg it is often described as a shooting pain, although some patients report numbness or tingling/burning sensation along the nerve path in the leg

Answer 316

herniated disc, sponylolisthesis, spinal stenosis

Answer 317

Age Obesity Occupation Prolonged sitting Diabetes

Answer 318

Sciatic stretch test - can’t perform straight leg raise test without pain Spinal MRI (GS)

Answer 319

Analgesia + physiotherapy Neuropathic med if symptoms persisting/worsening - amitriptyline, duloxetine Neurosurgery

Answer 320

Increased intracranial pressure which occurs when a brain injury or other problem causes the brain to press on the skull

Answer 321

- hydrocephalus - traumatic haematomas - tumours (glioma, meningioma) - abscess - focal oedema secondary to trauma, infarction, tumour - obstruction to major venous sinuses - diffuse brain oedema or swelling e.g. encephalitis, meningitis, SAH, near drowning - idiopathic intracranial hypertension

Answer 322

Headache Blurred vision, pupillary changes Vomiting Confusion Hypertension Shallow breathing Changes in behaviour - slow decision making, abnormal social behaviour Weakness or mobility problems (hemiparesis) Fatigue, drowsiness

Answer 323

papilledema

Answer 324

fixed dilated pupil result of unopposed pressure on parasympathetic fibres on the outside of the oculomotor nerve (CNIII) leading to there being only sympathetic innervation of the iris --> pupil is constantly dilated

Answer 325

Nervous system examination GCS assessment Spinal tap (measure the pressure of cerebrospinal fluid) CT scan MRI

Answer 326

Anticonvulsants to manage seizures CSF drainage using an intraventricular catheter Head of bed elevation Analgesia and sedation (usually with propofol, etomidate or midazolam and morphine or alfentanil) Neuromuscular blockade Treat underlying cause

Answer 327

brain herniation - when the ICP is so great that is forces brain tissue through one of the rigid intracranial barriers (tentorial notch, falx cerebri, foramen magnum)

Answer 328

Systolic hypertension with a triad of increased pulse pressure, irregular respirations and bradycardia as a result of raised ICP

Answer 329

a state of profound unconsciousness caused by disease, injury or poison

Answer 330

unresponsive and unrousable closed eyes depressed brainstem reflexes (e.g. unresponsive pupils) no limb response except reflex movements no response to painful stimuli except for reflexes irregular breathing

Answer 331

Using the Glasgow coma scale: 3 - indicates deep coma or death <8 - severe reduction in consciousness and patient unlikely to be able to maintain their airway spontaneously - require intubation and ventilation Using the AVCPU scale - unresponsive

Answer 332

resuscitation with intubation and ventilation + rehydration (if needed) intravenous thiamine and glucose (for patients without clear diagnosis) trial naloxone or flumazenil treat underlying cause raised ICP may require mannitol infusion

Answer 333

where patients have lost cognition and external awareness, but retain non-cognitive brain function and normal or near-normal sleep-wake cycle

Answer 334

narrowing of the spinal canal or neural foramina producing root ischaemia and neurogenic claudication (muscle pain due to lack of oxygen which is triggered by activity and relieved by rest)

Answer 335

Congenital narrowing of the spinal cord Hyperparathyroidism Paget's disease of bone Ankylosing spondylitis Cushing's syndrome Acromegaly

Answer 336

degenerative arthritis of the spine

Answer 337

neck pain with restricted ROM of the neck (cervical spine stenosis) gait instability loss of fine motor control of the upper limbs weakness and sensory disturbance in the upper and lower limbs urinary urge incontinence

Answer 338

lumbar spine XR lumbar spine MRI CT myelography if MRI unavailable

Answer 339

Cauda equina syndrome Peripheral arterial disease Spinal tumours Large central disc herniation Spondylolisthesis Lumbar spine trauma

Answer 340

NSAIDs, physiotherapy and epidural steroid injections Surgery - occasionally indicated for patients not responding to conservative measures however there is currently little evidence on the efficacy of surgery in treating lumbar spinal stenosis

Answer 341

a chronic neurological disorder in which the brain loses its normal ability to regulate the sleep-wake cycle

Answer 342

Type 1 narcolepsy involves cataplexy and patients have low levels of orexin in their CSF Type 2 does not involve cataplexy (more common, 80%)

Answer 343

a sudden loss of voluntary muscle tone with preserved consciousness, triggered by emotion

Answer 344

- severity can vary e.g. from barely susceptible slackening of the facial muscles, dropping of the jaw or the entire head, to weakness at the knees or collapse onto the floor - slurred speech and visual symptoms - intact hearing, awareness and consciousness - variable frequency - usually bilateral weakness

Answer 345

aged 10-30 family history traumatic brain injury certain HLA subtypes

Answer 346

excessive daytime sleepiness (EDS) disrupted nighttime sleep and/or vivid dreams cataplexy caused by muscle atonia hypnagogic/hypnopompic hallucinations sleep paralysis

Answer 347

polysomnography multiple sleep latency testing CSF orexin levels

Answer 348

obstructive sleep apnoea sleep deprivation automatism sleep paralysis

Answer 349

- good sleep hygiene - scheduled naps - central nervous system stimulants (1st line: modafinil) - antidepressants (for cataplexy) e.g. clomipramine, SSRIs, venlafaxine - sodium oxybate (potent sedative which improves nocturnal sleep quality) - support and modifications (with school/work)

Answer 350

also known as herpes zoster virus, shingles is a disease which triggers a painful skin rash in a dermatomal distribution

Answer 351

human herpesvirus-3 primary infection usually occurs in childhood, producing chickenpox (varicella) after this the virus lies dormant in the sensory nervous system but is susceptible to reactivation in patients over 50 years old and is associate with immunosuppressive illness, or psychological/physical trauma

Answer 352

increased age (50+) immunocompromise HIV, Hodgkin's lymphoma and bone marrow transplants

Answer 353

Pre-eruptive phase - itching, burning and paresthesia of single dermatome with flu-like symptoms but no visible rash Eruptive phase - appearance of skin lesions which form crusts over 7-10 days, accompanied by acute neuritic pain Chronic phase - postherpetic neuralgia - persistent or recurring pain lasting 30+ days after acute infection

Answer 354

usually clinical diagnosis based on typical lesions in a single dermatome PCR test, Tzanck smear

Answer 355

atopic eczema, eczema herpeticum, contact dermatitis, herpes simplex or impetigo

Answer 356

rash care oral acyclovir analgesia

Answer 357

An umbrella term which encompasses a group of permanent movement and posture disorders which limit activity

Answer 358

Spastic type - intermittently increased tone and pathological reflexes Athetoid - characterised by increased activity (hyperkinesia) Ataxic type - loss of orderly muscular coordination so that movements are performed with abnormal force, rhythm or accuracy Mixed - there may be a combination of several forms

Answer 359

- acquired pathology within the developing brain during the prenatal or early infant period - the impaired movement associated with CP results from centrally-mediated abnormal muscle tone which leads (most commonly) to spasticity - the main causes are prematurity, multiple gestation, and maternal infection

Answer 360

preterm birth congenital malformations multiple births intrauterine infections chorioamnionitis toxic or teratogenic agents

Answer 361

low birth weight neonatal encephalopathy neonatal sepsis intraventricular haemorrhage

Answer 362

meningitis intracranial haemorrhage trauma infection hyperbilirubinaemia hypoxia seizures

Answer 363

- low Apgar score 5 mins post birth - delayed developmental milestones - abnormalities of posture and movement are common throughout the different types of cerebral palsy - unusual fidgety movements or other abnormalities of movement, including asymmetry or paucity of movement - abnormalities of tone, including hypotonia, spasticity or dystonia abnormal motor development, including late head control, rolling and crawling - feeding difficulties - non motor problems such as learning disabilities, difficulties with communication, emotion and behaviour, visual impairment, pain

Answer 364

diagnosis is based on clinical examination and parental observations also: - thyroid studies - chromosomal analysis - MRI/CT

Answer 365

Acute poliomyelitis Becker's muscular dystrophy Charcot-Marie-Tooth disease Kugelberg-Welander spinal muscular atrophy Neonatal brachial plexus palsies Stroke motor impairment

Answer 366

Different for every individual Significant involvement of physios, OTs, speech therapists and recreational therapists Mobility aids, splinting Oral diazepam or baclofen in children and young people if spasticity is contributing to discomfort or pain, muscle spasms or functional disability

Answer 367

also known as von Recklinghausen's disease genetic disorder causing lesions in the skin, nervous system and skeleton

Answer 368

a defect in the gene NF1 - neurofibromin, the gene product, is a ubiquitous nervous system protein and is believed to act as a tumour suppressor - loss of neurofibromin leads to an increased risk of developing benign and malignant tumours but the effects of a mutation are very variable and can appear at any age due to a variety of mutations, differing penetration and mosaicism

Answer 369

- Cafe au lait spots - Neurofibromas - Freckling - Optic glioma - ≥2 Lisch nodules - Bone lesions - [1st degree relative with NF1] not a symptoms but a diagnostic criterion

Answer 370

Usually clinically diagnosed MRI CT/XR

Answer 371

no curative treatment symptomatic neurofibromas are often removed, or in some cases treated neurologically many patients have hundreds of cutaneous lesions so it is not possible or practical to removed them all genetic counselling should be given to all patients

Answer 372

a much rarer, central form of neurofibromatosis with CNS tumours rather than skin lesions

Answer 373

a recently recognised form of neurofibromatosis, characterised by multiple non-cutaneous schwannomas

Answer 374

a rare condition which results from disruption to the sympathetic nerves supplying the eye

Answer 375

partial ptosis (upper eyelid drooping) miosis (pupillary constriction) hemifacial anhidrosis

Answer 376

Stroke Multiple Sclerosis Swelling Syringomyelia (cyst in the spinal cord)

Answer 377

Tumour (Pancoast tumour) Trauma Thyroidectomy Top rib

Answer 378

Carotid aneurysm Carotid artery dissection Cavernous sinus thrombosis Cluster headache

Answer 379

guided by suspected cause CXR CT/MRI CT angiography/carotid USS Pharmacological testing

Answer 380

Horner's syndrome is a physical sign so management involves diagnosis of the underlying condition and treatment specific to diagnosis

Answer 381

a condition causing sudden weakness in the muscle on one side of the face

Answer 382

herpes simplex herpes zoster EBV cytomegalovirus infections adenoviruses rubella mumps influenza B coxsackievirus

Answer 383

20-50 yr olds pregnancy diabetes mellitus hypertension obesity

Answer 384

the nerve that controls facial muscles passes through a narrow corridor of bone on its way to the face in Bell's palsy that nerve becomes inflamed and swollen - usually related to a viral infection

Answer 385

rapid onset unilateral facial nerve weakness generalised weakness of affected side severe cases may also present with notable loss of taste sensation (classically anterior 2/3 of tongue), intolerance of high-pitched noises, mild dysarthria lower motor neuron signs (forehead affected, unlike in UMN lesions where there is forehead sparing)

Answer 386

usually clinically diagnosed, based on the clinical signs House-Brackmann scale is occasionally used to describe the degree of paralysis (scale 1-6, 1 is normal, 6 is total paralysis)

Answer 387

Ramsay-Hunt syndrome Guillain-barre syndrome Lyme disease

Answer 388

steroids - prednisolone antivirals - acyclovir eye-care - reduced eye closing can lead to dry eye and corneal damage

Answer 389

a condition caused by lesions in the motor nuclei of the medulla, so called bulbar palsy because this region of the brain is sometimes called the 'bulb' of the brainstem

Answer 390

MND Guillain-Barre Syndrome Polio Syringobulbia Brainstem tumours Myasthenia gravis Myotonic dystrophy

Answer 391

Tremulous lips Weak and wasted tongue which fasciculates in the mouth (‘bag of worms’) Drooling Absent palatal movements Dysphonia Articulation - difficulty pronouncing r; unable to pronounce consonants as dysarthria progresses If the pathology progresses then speech becomes slurred and eventually becomes indistinct There may also be neurological deficits in the limbs - e.g. flaccid tone, weakness with fasciculations

Answer 392

electromagnetic articulography (EMA) electropalatography (EPG) pressure sensing EPG routine bloods, brain/brainstem imaging, electromyography

Answer 393

treatment is directed to underlying cause postural changes can help with drooling of saliva and may prevent aspiration supportive measures support from SALT and dieticians

Answer 394

a clinical condition involving one or more nerves resulting in impaired function (neuropathy)

Answer 395

degenerative disc disease osteoarthritis facet joint degeneration/hypertrophy ligamentous hypertrophy certain injuries e.g. car accident trauma less common causes include injury by tumours and diabetes

Answer 396

female caucasian smoking

Answer 397

depends on nerves affected most common symptoms; - pain - numbness - tingling

Answer 398

ice or heat adjusting posture or physiotherapy OTC NSAIDs corticosteroids surgery

Answer 399

a disorder of the inner ear caused by a change in the fluid volume in the labyrinth

Answer 400

exact cause in unknown but thought to be a multifactorial and linked to: - Allergy - Autoimmunity - Genetic susceptibility - Metabolic disturbances involving the balance of sodium and potassium in the fluid of the inner ear - Vascular factors - Viral infection, otosyphilis, Cogan’s syndrome (non-syphilitic interstitial keratitis and bilateral audiovestibular deficits

Answer 401

- vertigo - tinnitus - fluctuating hearing loss with a sensation of aural pressure

Answer 402

- acute attacks typically last mins-hrs - acute episodes may occur in clusters of around 6-11 per year - remission of symptoms may last several months - most patients develop unilateral symptoms initially with bilateral symptoms sometimes developing later

Answer 403

bloods audiometry visual nystagmography MRI

Answer 404

Acoustic neuroma Otitis media Earwax Ototoxic drugs Intracranial pathology e.g. tumours, migraine Systemic illness e.g. anaemia, hypothyroidism

Answer 405

alleviate acute attacks, reduce severity and frequency of attacks, improve hearing reduce the impact of tinnitus

Answer 406

motion sickness medications (meclizine, diazepam) antinausea medications (promethazine) diuretics (furosemide, chlorthalidone) middle ear injections (gentamicin)

Answer 407

endolymphatic sac procedure (help with decompression) vestibular nerve section (helps to correct vertigo and maintain hearing) labyrinthectomy (removal of labyrinth)

Answer 408

hearing aids vestibular rehab therapy low sodium diet avoid caffeine, alcohol

Answer 409

also known as temporal arteritis A type of systemic vasculitis affecting the medium and large arteries, there is a strong link with polymyalgia rheumatica

Answer 410

Unilateral headache typically severe and around the temple and forehead Can be associated with: Scalp tenderness Jaw claudication Blurred or double vision Loss of vision if untreated

Answer 411

Symptoms of polymyalgia rheumatica Systemic symptoms (e.g. weight loss, fatigue and low-grade fever) Muscle tenderness Carpal tunnel syndrome Peripheral oedema

Answer 412

usually clinically diagnosed Inflammatory markers Temporal artery biopsy (showing multinucleated giant cells) Duplex USS (showing the hypoechoic “halo” sign and stenosis of the temporal artery

Answer 413

Steroids are the main treatment and started immediately even before diagnosis is confirmed to reduce the risk of vision loss * 40-60mg prednisolone with no visual symptoms or jaw claudication * 500-1000mg methylprednisolone with visual symptoms/jaw claudication Once diagnosis is confirmed and the condition is controlled, the steroid dose is slowly weaned over 1-2 years Other medications include: - Aspirin - PPI for gastric protection on steroids - Bisphosphonates and calcium and vitamin D for bone protection on steroids

Answer 414

Visual loss Steroid -related complications e.g. cushingoid symptoms Cerebrovascular accident e.g. stroke

Answer 415

also known as chronic fatigue syndrome A complex, chronic medical condition affecting multiple body systems and of unknown cause which has many different presentations

Answer 416

Underlying cause is not well understood Approximately 50-80% of people with ME start suddenly with a flu-like illness Often found after infection suggesting an immunological dysfunction Strong genetic predisposition Life stressors

Answer 417

Debilitating fatigue Post-exertional malaise Unrefreshing sleep or sleep disturbance ‘Brain fog’ Significantly reduced ability to engage in occupational, educational, social or personal activities

Answer 418

Orthostatic intolerance and autonomic dysfunction (e.g. dizziness, palpitations, fainting…) Temperature hypersensitivity Neuromuscular symptoms Flu-like symptoms Intolerance to alcohol Heightened sensory sensitivities Pain

Answer 419

Postural tachycardia syndrome Hypothyroidism, diabetes, anaemia Metabolic muscle disorders Psychiatric illness

Answer 420

Lifestyle advice - pace yourself, rest as needed, maintain health diet, work adjustments CBT

Answer 421

a rare non-cancerous tumour which grows slowly from overproduction of schwann cells. It presses on the hearing and balance nerves in the inner ear and causes hearing loss and other auditory symptoms

Answer 422

a seizure accompanied by fever (temperature >38 degrees) without CNS infection, which occurs in infants and children aged 6mo-6yrs

Answer 423

simple = isolated, generalised, tonic-clonic seizures lasting <15 mins and don't recur within 24 hrs of with same febrile illness, complete recovery in 1 hr complex= 1 or more of a partial seizure, duration of 15+ mins, recurrence within 24 hrs or within same febrile illness and in complete recovery within 1 hr

Answer 424

peripheral nerve damage as a result of diabetes mellitus most commonly resulting in pain, burning, tingling or numbness in the toes or feet and extreme sensitivity to light touch

Answer 425

control of blood sugar levels lifestyle interventions, specifically diet and exercise care for the feet to prevent complications control of pain caused by neuropathy

Answer 426

an incomplete spinal cord injury which is often related to flexion injuries of the cervical region which result in infarction of the anterior 2/3s of the cord and/or its vascular supply from the anterior spinal artery

Answer 427

impairments in the pain and temperature sensations bilaterally while vibratory and proprioceptive sensations are preserved the corticospinal tracts are also likely to have been affected resulting in bilateral spastic paralysis and UMN signs

Answer 428

also called central cord syndrome occurs due to the development of a fluid filled cyst (a syrinx) around the spinal canal

Answer 429

- the pattern of deficit seen in patients with syringomyelia initially seems confusing as it is different from other syndromes - the upper limbs are affected first whilst the lower limbs are spared until much later - as the cervical cord is the most likely location of the lesion, there is classically said to be a "cape-like" loss of pain and temperature sensation

Answer 430

abnormal build up of CSF within the brain and spinal cord, this is a result of either over-production of CSF or a problem with draining or absorbing CSF

Answer 431

CSF is created in the four choroid plexuses (one in each ventricle) and by the walls of the ventricles CSF is absorbed in to the venous system b the arachnoid granulations

Answer 432

Non-communicating/obstructive - the flow of CSF is obstructed within the ventricles or between the ventricles and the subarachnoid space Communicating - there is communication between the ventricles and the subarachnoid space and the problem lies outside of the ventricular system (e.g. due to reduced absorption or blockage of the venous drainage system), may also be due to increased CSF production

Answer 433

ventricular dilatation in the absence of raised CSF pressure

Answer 434

gait abnormality urinary incontinence dementia

Answer 435

neuroimaging large-volume lumbar puncture intraventricular pressure monitoring lumbar infusion test (intrathecal test)

Answer 436

Medical = Carbonic anhydrase inhibitors (acetazolamide) and repeated lumbar puncture Surgical = ventriculo-peritoneal shunt insertion (1st line), ventriculo-atrial shunt is an alternative

Neurology Flashcards

(463 cards)