The Brain Flashcards

Question

Define Guillain-Barre Syndrome

Answer 1

Acute paralytic polyneuropathy that affects the peripheral nervous system

Answer 2

Molecular mimicry B cells create antibodies against the antigens on the triggering pathogen Antibodies match proteins on the peripheral neurones May target proteins on the myelin sheath or the nerve axon itself

Answer 3

More common in males > 50 years

Answer 4

Usually triggered by an infection Gastroenteritis or influenza like illness before onset of neurological symptoms

Answer 5

Preceding: viral illness bacterial infection mosquito-borne viral infection Hepatitis E infection

Answer 6

Usually start within 4 weeks of triggering infection Symptoms peak 2-4 weeks - Begin in the feet and progress upwards - Acute, symmetrical, ascending weakness - sensory symptoms - reduced reflexes

Answer 7

Nerve conduction studies Lumbar puncture for CSF

Answer 8

Brighton criteria

Answer 9

Diagnostic tool - helps identification and monitoring Help distinguish low and high-risk patients

Answer 10

Clinical (Brighton criteria) = supporting investigations

Answer 11

Syndrome characterised by motor difficulty, absence of deep tendon reflexes, Paraesthesias without objective sensory loss and increased CSF albumin with a normal cell count

Answer 12

IV immunoglobulins

Answer 13

1st line - immunoglobulins Supportive care VTW prophylaxis

Answer 14

Transverse myelitis Myasthenia gravis Botulism Polymyositis Vasculitis neuropathy

Answer 15

Pulmonary embolism

Answer 16

Recovery can take months to years. Can continue regaining function 5 years after acute illness. Either full recovery or minor symptoms. Some left with significant mortality

Answer 17

5% Mainly due to respiratory or cardiovascular complications

Answer 18

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

Answer 19

Unknown Selective loss of nigrostriatal dopaminergic neurones in the substantia nigra pars compacta Intracytoplasmic eosinophilic inclusions (Lewy bodies) and neuritis

Answer 20

Bradykinesia

Answer 21

Older age - 70 years Male Gradual onset of symptoms

Answer 22

Sporadic Unknown - Genetic predisposition - Environmental factors/exposures

Answer 23

Increasing age History of familial PD in younger-onset disease Mutation in gene encoding glucerebrosidase

Answer 24

Asymmetrical Resting tremor - a tremor worse with rest Rigidity - resisting passive movement Bradykinesia - slowness of movement

Answer 25

Stooped posture Facial masking Forward tilt Reduced arm swing Shuffling gait

Answer 26

Multiple system atrophy Dementia with Lewy bodies

Answer 27

Dopaminergic agent trial - improvement of symptoms

Answer 28

History + examination findings

Answer 29

No cure Treatment options - Levodopa - COMT inhibitors - Dopamine agonists - Monoamine oxidase B-inhibitors

Answer 30

Essential tremor Multiple system atrophy Dementia with Lewy bodies Corticobasal degeneration Alzheimer's disease with parkinsonism

Answer 31

Levodopa-induced dyskinesias Motor fluctuations Dementia Constipation Bladder dysfunction Orthostatic hypotension Sleep disorders Dysphagia

Answer 32

Course is progressive Unilateral symptoms become bilateral After 5 years - motor complications develop

Answer 33

Autosomal dominant genetic condition that causes progressive neurological dysfunction

Answer 34

CAG repeat generates elongated polyglutamine tail of the huntingtin protein. Leads to cleavage and generation of toxic fragments of this abnormal protein Toxic fragments can cross-link Forms aggregates that resist degradation, interfere with normal cell function

Answer 35

Symptoms begin aged 30-50 Men and women equally

Answer 36

Autosomal dominant Trinucleotide repeat disorder CAG HTT gene mutation of chromosome 5 - encodes for huntingtin (HTT) protein

Answer 37

Successive generations have more repeats in the gene Results in: Earlier age of onset Increased severity of disease

Answer 38

Expansion of CAG repeat in huntingtin gene Family history

Answer 39

Insidious, progressive worsening of symptoms Typically, begins with cognitive, psychiatric or mood problems, followed by development of movement disorders

Answer 40

Chorea Dystonia Rigidity Eye movement disorders Dysarthria Dysphagia

Answer 41

No initial tests Genetic testing - CAG repeat testing MRI or CT scan

Answer 42

Genetic testing (with pre and post-test counselling)

Answer 43

No treatment options for slowing or stopping progression

Answer 44

Genetic counselling MDT Physiotherapy Speech and language therapy Tetrabenazine Antidepressants Advanced directives End-of-life care

Answer 45

Tardive dyskinesia DRPLA Neuroacanthocytosis Spinocerebellar ataxia 17

Answer 46

Progressive condition Life expectancy 10-20 years after onset of symptoms Progresses - more frail and susceptible to illness Death often due to aspiration pneumonia Suicide common

Answer 47

Weight loss Dysphagia Falls Suicide risk

Answer 48

Fever, photophobia or neck stiffness Sudden-onset occipital headache Postural, worse on standing, lying or bending over Vomiting History of trauma or cancer Pregnancy

Answer 49

Complex neurological disorder causing episodes or attacks of headache and associated symptoms

Answer 50

Results from neurological inflammation of first division trigeminal sensory neurones that innervate the large vessels and meninges in the brain When trigeminal neurones are activated - release substances that cause dilation of meningeal blood vessels, leakage of plasma proteins into surrounding tissue and platelet activation

Answer 51

Waves of excitation spread anteriorly in the cortex followed by a prolonged period of decreased neuronal activity then neuronal recovery Results in activation of nociceptors in adjacent dura and blood vessels Leads to activation of trigeminal sensory nucleus

Answer 52

1. Migraine with aura 2.Migraine without aura 3. Silent migraine - migraine with aura without headache 4. Hemiplegic migraine

Answer 53

Very common Affect women more than men Common among teenagers and young adults

Answer 54

Genetic factors Brain of people who experience migraines = hyperexcitable to a variety of stimuli

Answer 55

1. Premonitory or prodromal stage 2. Aura 3. Headache stage 4. Resolution stage 5. Postdromal or recovery phase

Answer 56

Can begin several days before the headache Could be yawning, fatigue or mood change

Answer 57

Lasts up to 60 minutes Can affect vision, sensation or language

Answer 58

Lasts 4-72 hours Main features - unilateral - moderate-severe intensity - pounding or throbbing nature - photophobia - phonophobia - osmophobia - aura - nausea and vomiting

Answer 59

Headache may fade away or be relieved abruptly by vomiting or sleeping

Answer 60

= clinical diagnosis Headache diary may be useful

Answer 61

Stress Bright lights Strong smells Certain foods Dehydration Mensuration Disturbed sleep Trauma

Answer 62

By international classification of headache disorders (ICHD)- 3 criteria for migraines

Answer 63

At least 5 or more attacks in a lifetime Headache attack lasting 4-72 hours

Answer 64

Having full reversible visual symptoms, sensory symptoms or dysphasic speech disturbance

Answer 65

Retreat to dark, quiet room, sleeping Medical - NSAIDs - Paracetamol - Triptans - Antiemetics NO opioids

Answer 66

Depends on the frequency and severity of the attacks Usual: - propranolol - amitriptyline - topiramate Other - cognitive behavioural therapies - mindfulness and medication - acupuncture - vitamin B12

Answer 67

Headache tension Headache cluster Medication-overuse headache Headache after head or neck trauma Subarachnoid haemorrhage

Answer 68

Key features - hemiplegia - ataxia - impaired consciousness Autosomal dominant or no genetic link Can mimic a stroke/TIA

Answer 69

Combined pill

Answer 70

Tend to become less frequent and severe or stop altogether with time - particularly after menopause Slight increase in risk - especially with aura

Answer 71

Not fully understood Similar to migraine - central hypersensitivity Chronic = state of generalised hyperalgesia.

Answer 72

Stress Depression Alcohol Skipping meals Dehydration

Answer 73

Very common Episodic = most common type of headache Most common between 20-39

Answer 74

Involvement of peripheral factors - pericranial muscles Genetic factors, specific genes = unknown Common trigger = psychological stress

Answer 75

Mental tension Stress Missing meals Fatigue Lack of sleep

Answer 76

Either episodic or chronic Mild ache or pressure in band-like pattern around head - dull - non-pulsatile - bilateral - pressing/pressure-like pain - pericranial tenderness = common No visual changes Develop gradually

Answer 77

History + physical examination Headache diaries can help

Answer 78

Amitriptyline

Answer 79

1st line = amitriptyline - reassurance - simple analgesia - non-drug therapies

Answer 80

Chronic migraine Medicine overuse headache Sphenoid sinusitis Giant cell arteritis Temporomandibular disorder Pituitary tumour

Answer 81

Depression, anxiety, poor sleep and stress - potential of poor prognosis

Answer 82

Tension headaches do not have: Significant nausea No vomiting Little or no photophobia or phonophobia Lack of aggravation by routine physical activity

Answer 83

1. Trigeminal disruption of the pain 2. Ipsilateral cranial autonomic symptoms 3. Circadian/circannual pattern of attacks

Answer 84

Physiological reflex arc, the trigeminal autonomic reflex. Increased firing of parasympathetic nerve fibres (trigeminal nerve) innervating facial structures - causes autonomic features seen in an attack

Answer 85

30-50 year old male Male Smoker

Answer 86

Unknown - potentials: Head trauma Heavy cigarette smoking Heavy alcohol intake

Answer 87

Male sex Family history Head injury Cigarette smoking Heavy drinking

Answer 88

Severe and unbearable unilateral headaches - usually around the eye Clusters of attacks then disappear for extended periods 'Suicide headache' due to severity

Answer 89

Red, swollen and watering eye Pupil constriction (miosis) Eyelid dropping (ptosis) Nasal discharge Facial sweating

Answer 90

Brain and pituitary MRI without and with intravenous contrast Erythrocyte sedimentation rate

Answer 91

Alcohol Strong smells Exercise

Answer 92

Prophylaxis - verapamil Prevent attacks

Answer 93

Triptans High flow 100% oxygen

Answer 94

Migraine Paroxysmal hemicrania Trigeminal neuralgia Cluster-tic syndrome Angel-closure glaucoma Subarachnoid haemorrhage Giant cell arteritis

Answer 95

Inflammation of the meninges, usually due to an infection

Answer 96

When the bacteria infect the meninges and the CSF

Answer 97

When meningococcus bacterial infection is the blood stream. Can cause a non blanching rash

Answer 98

Bacterial Viral

Answer 99

Neisseria meningitidis Streptococcus pneumonia Group B streptococcus (neonates) Listeria monocytogenes (neonates)

Answer 100

Enterovirus Herpes simplex virus (HSV) Varicella zoster virus (VZV)

Answer 101

Most = young age Winter season Absent/non-functioning spleen Older age > 65 Immunocompromised Incomplete immunisation Cancer Smoking

Answer 102

Infants and young children Young adults Older people Summer and autumn Exposure to mosquito or tic vector Unvaccinated for mumps

Answer 103

Fever Neck stiffness Vomiting Headache Photophobia Altered consciousness Seizures Non-blanching rash

Answer 104

Meningococcal septicaemia

Answer 105

Lumbar puncture Viral PCR testing on CSF sample Blood culture Meningococcal PCR Kernig's test Brudzinski's test

Answer 106

Insert needle into lower back CSF at L3-4 or L4-5 intervertebral space Samples sent for bacterial culture, viral PCR, cell count, protein and glucose Blood glucose sent at same time

Answer 107

Kernig's test Brudzinski's test

Answer 108

Lay patient on back, flex one hip and knee to 90 degrees Slowly straighten the knee while keeping hip flexed at 90 Created slight stretch in the meninges If meningitis = produce spinal pain or resistance to movement

Answer 109

Lie patient flat on back, gently using hands to life head and neck of bed, flexing chin to chest Positive test = causes patient to flex their hips and knees involuntary

Answer 110

Blood cultures and lumbar puncture before antibiotics Aciclovir - viral meningitis (HSV, VZV) Bacterial - steroids - benzylpenicillin

Answer 111

Steroids Benzylpenicillin

Answer 112

Significant exposure to meningococcal infection puts contacts at risk Highest risk within 7 days of onset of illness Single dose = ciprofloxacin

Answer 113

Bacterial/viral Encephalitis Encephalopathy Drug induced meningitis TB meningitis

Answer 114

Hearing loss - key Seizure and epilepsy Cognitive impairment Memory loss Focal neurological defects

Answer 115

Facial pain syndrome in the distribution of 1 or more divisions of the trigeminal nerve

Answer 116

Cause intense facial pain in the distribution of the trigeminal nerve 90% cases are unilateral

Answer 117

Ophthalmic nerve (V1) Maxillary (V2) Mandibular (V3)

Answer 118

Multiple sclerosis

Answer 119

Focal demyelination and the resultant conduction aberrations

Answer 120

Majority of patients - focal compression of the trigeminal nerve root at the entry zone by an aberrant vascular loop Multiple sclerosis - demyelinating plaques in the pons that encompass the root entry zone of the trigeminal nerve

Answer 121

Increased age Multiple sclerosis

Answer 122

Pain comes on suddenly can last seconds to hours Electricity like Shooting Stabbing Burning pain

Answer 123

Touch Eating Shaving Cold

Answer 124

Clinical + history of paroxysms of sharp, stabbing, intense pain lasting up to 2 minutes

Answer 125

Carbamazepine

Answer 126

1st line = carbamazepine Medical therapies Vascular decompression Ablative decompression Surgical interventions

Answer 127

Dental caries/fractures Mandibular osteomyelitis Migraine Temporomandibular joint syndrome Glossopharyngeal neuralgia

Answer 128

Chronic neurodegenerative disease with an insidious onset and progressive but slow decline

Answer 129

Vascular dementia

Answer 130

Reduced brain weight Cortical atrophy in temporal, frontal and partial area Changes in senile plaques and neurofibrillary tangles seen Beta-amyloid induced injury to brain cells.

Answer 131

Abundance of tangles is roughly proportional to the severity of clinical disease and cognitive decline

Answer 132

Amyloid plaques - clumps of beta-amyloid Neurofibrillary tangles

Answer 133

Advanced age Family history Genetics Down's syndrome Cerebrovascular disease Lifestyle factors and medications Less than secondary school education

Answer 134

Memory loss Impairment of daily activities Neurobehavioral abnormalities

Answer 135

Bedside cognitive testing MRI or CT Tests to rule out other conditions

Answer 136

Assess and manage other long-term conditions Possible referral AChE inhibitors Reduce polypharmacy

Answer 137

Pneumonia Institutionalisation UTI Falls and their complications Weight loss Elder abuse

Answer 138

Primary neurodegenerative brain disease in adults > 65 years of age. Spectrum compromises a heterogenous group of conditions that are heritable in some cases

Answer 139

Frontal lobar degeneration - neural loss, gliosis and microvascular changes of frontal lobes, anterior temporal lobes, anterior cingulate cortex and insular cortex Several subtypes

Answer 140

According to main protein component of neuronal and glial abnormal inclusions and their distributions

Answer 141

Average age of onset 45-65 years Peak prevalence 7th decade Affects both sexes equally Average life expectancy post diagnosis = 8 years

Answer 142

Neuron damage and death occurring in frontal and temporal lobes Atrophy - due to deposition of abnormal proteins (tau protein) Genetic component 1/4 cases

Answer 143

Mutations in: MAPT gene CRN gene C9orf72 gene

Answer 144

Behavioural presentation Semantic presentation Non fluent presentation

Answer 145

Formal cognitive testing Imaging - brain MRI or CT

Answer 146

No cure Care plan Medicine - antidepressants - antipsychotics Other support End of life plans

Answer 147

Other forms of dementia Bipolar disorder Major depression OCD Primary brain tumour Hyperthyroidism

Answer 148

Shorter survival and faster rates of cognitive and functional decline that patients with Alzheimer's disease

Answer 149

Neurodegenerative disorder with parkinsonism, progressive cognitive decline, prominent executive dysfunction, behavioural and sleep disturbances and visuospatial impairment

Answer 150

Accumulation of lewy bodies at vulnerable sites Lewy bodies - composed of protein alpha-synuclein - cytoplasmic protein associated with synaptic vesicles Normal function of this protein - role in transportation of synaptic vesicles and synaptic plasticity Distribution linked to clinical symptoms

Answer 151

> 50 Affects men slightly more than women Rapid progression Death 7 years post diagnosis

Answer 152

Spherical lewy proteins (alpha-synuclein) deposited in the brain Toxic protein aggregation Abnormal phosphorylation

Answer 153

Parkinson's = deposited in substantia nigra Lewy body dementia = more widespread

Answer 154

Cognitive fluctuations Recurrent visual hallucinations Rapid eye movement (REM) sleep behaviour disorder + one or more spontaneous cardinal motor features of Parkinsonism.

Answer 155

Serum thyroid stimulating hormone Serum vitamin B12 Ct head MRI head

Answer 156

Clinical + confirmed pathologically presence of Lewy bodies

Answer 157

1st line pharmacological = cholinesterase inhibitors Other medications Main goal = improve or stabilise cognition, behaviour, and activities of family living and to maintain safety

Answer 158

Cholinesterase inhibitors

Answer 159

Alzheimer's disease Parkinson's disease Frontotemporal dementia Vascular dementia Prion disorders

Answer 160

Progressive Treatment = symptomatic Mean survival 5 years

Answer 161

Chronic progressive disease of the brain characterised by a chronic progressive multifaceted impairment of cognitive function

Answer 162

Large - affect individual regions, will exhaust the brain's compensatory mechanisms and lead to dementia Small - in strategic areas

Answer 163

Causes white matter pallor to naked eye Loss of axons, myelin and oligodendrocytes Perivascular tissue loss and dilation of perivascular spaces Damage to capillaries with breakdown of the BBB and protein leakage

Answer 164

Large parenchymal haemorrhages centred in basal ganglia (often due to hypertension) Multiple haemorrhages occur in cortex and white matter Angioplasty due to amyloid beta protein

Answer 165

Alzheimer's dementia + vascular dementia Act synergistically with each other Co-exist - affected to greater degree compared to only one pathology

Answer 166

More common in males Prevalence increases in those who have had a stroke

Answer 167

Most common = cerebrovascular infarcts Infarction Leukoriosis Haemorrhage

Answer 168

Age > 60 Obesity Hypertension - major Cigarette smoking Vascular risk factors

Answer 169

Progressive in step wise fashion Single infarct vascular disease - cognitive impairment following an event Motor and mood changes Mood disturbances

Answer 170

FBC Erythrocyte sedimentation rate Blood glucose level Renal and liver function tests Vitamin B12 Folate Thyroid function CT or MRI brain ECG

Answer 171

Early aggressive treatment of vascular risk factors Prevention of further cerebrovascular disease Supportive care Cholinesterase inhibitors Antihypertensives SSRIs Cognitive stimulation therapy Supportive care End of life care

Answer 172

Depression Alzheimer's disease Mild cognitive impairment Other forms of dementia Primary brain tumour

Answer 173

Depression Aggression Falls Stroke

Answer 174

Life expectancy significantly shortened - similar to AD

Answer 175

Describes transient monocular vision loss because of ischemia to retina, choroid or optic nerve (retinal transient ischaemic attack)

Answer 176

Due to narrowing (stenosis) or occlusion of the internal carotid artery or the central retinal artery Arterial embolus (atherosclerotic emboli) Thrombotic vascular events Inflammation of optic nerve Giant cell arteritis Diabetes, smoking, cocaine Hypertension - old age

Answer 177

Usually in retinal artery from ipsilateral carotid artery disease Accumulation of fat detaches from the inner lining of an artery and blocks blood flow elsewhere

Answer 178

> 50 Vascular risk factors - hypertension - hypercholesterolemia - smoking - previous history TIA/stroke

Answer 179

Typical presentation - transient vision loss in one or both eyes occurring abruptly Maximum severity within seconds and lasts seconds - followed by full visual recovery

Answer 180

Opthalamogical examination - typically normal Inflammatory markers (exclude) Carotid artery imaging Cardiac investigations

Answer 181

Aspirin Urgent referral

Answer 182

After diagnosis Statin therapy Antiplatelet therapy Optimising blood pressure control

Answer 183

Central retinal artery/vein occlusion Giant cell arteritis Multiple sclerosis Papilledema Epilepsy Sickle cell anaemia

Answer 184

Ischaemic stroke - 2% Death Adverse cardiac events

Answer 185

Untreated = major risk of stroke Carotid endarterectomy - good prognosis

Answer 186

Caused by compression of the lumbosacral nerve roots that extend below the spinal cord

Answer 187

Requires emergency decompression surgery to prevent permanent neurological dysfunction

Answer 188

Collection of nerve roots that travel through the spinal canal after the spinal cord terminates around L2/3. Nerve roots exit either side of their column at their vertebral level L3-5, S1-5 and Co. These nerves are compressed

Answer 189

Sensation to the lower limbs, perineum, bladder and rectum Motor innervation to the lower limbs, and the anal and urethral sphincters Parasympathetic innervation of the bladder and rectum

Answer 190

Herniated disc = most common Tumours - metastasis Spondylolisthesis Abscess - infection Trauma

Answer 191

Lumbar disc herniation Spinal trauma Spinal surgery Spinal epidural abscess Anticoagulation therapy

Answer 192

Presents LMN signs - reduced tone and reflexes Bladder dysfunction - always Other symptoms

Answer 193

Nerves being compressed are LMN that have already exited the spinal cord

Answer 194

MRI - ASAP CT lumbar spine

Answer 195

Lumbar decompression surgery Increases chance of regaining function

Answer 196

May still be left with bladder, bowel, sexual dysfunction, leg weakness and sensory impairment

Answer 197

Metastatic lesion compresses the spinal cord Presents similar to cauda equina Will be UMN signs - metastatic spinal cord compression is higher

Answer 198

Saddle anaesthesia Loss of sensation in the bladder and rectum Faecal incontinence Bilateral sciatica Bilateral or severe motor weakness in the legs Reduced anal tone on PR examination

Answer 199

Even with immediate decompression - patients still may not regain full function

Answer 200

Disorder that causes persistent feelings of low mood, low energy, and reduced interest

Answer 201

Multifactorial - biological, psychological, social Factors can be: predisposing, precipitating, perpetuating Often triggered by life events

Answer 202

Current employment Good social support Marital status being married

Answer 203

Not a single identifiable cause or trigger for cases of depression Biological factors Psychological factors Social factors

Answer 204

1. Low mood 2. Anhedonia - low interest or pleasure in most activities of the day 3. Lack of energy - anergia

Answer 205

Screening questions Investigations for exclude physical/organic causes

Answer 206

ICD-10/11 criteria

Answer 207

Mild depression = watchful waiting + advice about healthy habits. Follow up 2 weeks Severe depression = 1st line = antidepressant therapy + high-level psychosocial interventions Electroconclusive therapy

Answer 208

Bipolar affective disorder Premenstrual dysphoric disorder Bereavement Anxiety disorders Alcohol-use disorders

Answer 209

Hypothyroidism Cushing's disease or syndrome Vitamin B12 deficiency

Answer 210

Suicide risk - 4x higher Substance/alcohol misuse Recurrence of depressive episodes Reduced quality of life reduction Antidepressant side effects

Answer 211

Typically - lasts 3-6 months Most people recover within 12 months Illness episodic Feel well in-between acute depressive episodes

Answer 212

Encompasses a variety of specific diseases affecting motor nerves

Answer 213

Amyotrophic lateral sclerosis

Answer 214

Involves degeneration of both the upper and lower motor neurones Sensory neurones = spared

Answer 215

Late middle-aged e.g. 60 Man Possibly affected relative

Answer 216

Exact cause = unclear Genetic links Family history 10-15% Increased risk with smoking, exposure to heavy metals and certain pesticides

Answer 217

Genetic factors Lifestyle and environment - mechanical and/or electrical trauma - military service - high levels of exercise - exposure to agricultural chemicals - exposure to variety of heavy metals

Answer 218

Insidious, progressive weakness of muscles - first noticed in upper limbs Affects limbs, trunk, face and speech May be increased when exercising Clumsiness Slurred speech

Answer 219

Muscle wasting Reduced tone Fasciculations Reduced reflexes

Answer 220

Increased tone or spasticity Brisk reflexes Upgoing plantar reflexes

Answer 221

Clinical diagnosis + examination Electrophysiological studies

Answer 222

No effective management for halting or reversing the progression of the disease Riuzole Non-invasive ventilation Supporting person and their family

Answer 223

Affect on sensory neurones

Answer 224

Cervical spondylosis with myelopathy and radiculopathy Multifocal motor neuropathy Inclusion body myositis Myasthenia gravis Progressive muscular atrophy

Answer 225

Progressive - eventually fatal Tend to due of respiratory failure or pneumonia

Answer 226

Chronic autoimmune disorder of the post-synaptic membrane at the neuromuscular junction in skeletal muscle

Answer 227

Circulating antibodies against the nicotinic receptor or associated protein impair neuromuscular transmission

Answer 228

Affects men and women at different ages Women under 40 Men over 60

Answer 229

Acetylcholine receptor antibodies Muscle-specific kinase (MuSK) antibodies Low-density lipoprotein receptor-related protein 4 (LRP4) antibodies

Answer 230

Antibodies present at the neuromuscular junction

Answer 231

Important in creation and organisation of Ach receptor Destruction of these proteins leads to inadequate Ach receptors

Answer 232

Thymomas Family history of autoimmune disorders Genetic markers Cancer-targeted therapy

Answer 233

Thymus gland tumours 10-20% of patients have thymoma 30% patients with thymoma will develop mg

Answer 234

From mild to life-threatening severe Weakness that worsens with muscle use and improves with rest Symptoms better in morning, worse at end of day Affect proximal muscles of the limbs and small muscles of the head and neck

Answer 235

Examination - fatigue in muscles Look for thymectomy scar Forced vital capacity

Answer 236

AChR antibodies - around 85% MuSK antibodies - < 10% LRP4 antibodies - < 5%

Answer 237

CT or MRI of thymus gland Edrophonium test - helpful for diagnosis

Answer 238

Repeated blinking will exacerbate ptosis Prolonged upward gazing will exacerbate diplopia Repeated abduction of one arm 20x will result in unilateral weakness

Answer 239

Given IV edrophonium chloride Edrophonium blocks the enzymes which break down Ach at the neuromuscular junction Result = level of Ach at the neuromuscular junction rises - temporarily relieves the weakness Suggests diagnosis

Answer 240

Pyridostigmine Immunosuppression Thymectomy (even if do not have thymoma) Rituximab (last resort)

Answer 241

Lambert-eaton myasthenic syndrome Botulism Penicillamine-induced myasthenia gravis Primary myopathies

Answer 242

Potentially life-threatening Can cause acute worsening symptoms Respiratory muscle weakness - require non invasive ventilation or mechanical Treatment = IV immunoglobulin and plasmapheresis

Answer 243

Respiratory failure Impaired swallowing Acute aspiration Secondary pneumonia Cardiac complications

Answer 244

CNS - brain and spinal cord

Answer 245

Anywhere from the anterior horn cell to the muscle

Answer 246

Disuse atrophy or contractures Increased tone (spasticity/rigidity) +/- ankle clonus Pyramidal pattern of weakness Hyperreflexia Babinski sign

Answer 247

Occurs when stimulation of the lateral plantar aspect of the foot leads to extension

Answer 248

Marked atrophy Fasciculations Reduced tone Variable patterns of weakness Reduced or absent reflexes Down going plantars or absent response

Answer 249

Loss of inhibitory tone in muscles leads to constant contraction of muscles

Answer 250

Suppression by CNS, but the LMNs are damaged or lost, so there is nothing to tell the muscles to contract

Answer 251

Describe the event of temporarily losing consciousness due to a disruption of blood flow to the brain - often leading to a fall

Answer 252

Vasovagal episodes Fainting

Answer 253

Caused be a problem with the autonomic nervous system regulating blood flow to the brain When vagus nerve received a strong stimulus it can stimulate PNS PNS activation contracts SNS - blood vessels constricted As blood vessels delivering blood to the brain relax = hypoperfusion of brain tissue Leading to 'faint'

Answer 254

Dehydration Missed meals Extended standing in a warm environment A vasovagal response to a stimulus

Answer 255

Hypoglycaemia Dehydration Anaemia Infection Anaphylaxis Arrythmias

Answer 256

Simply fainting

Answer 257

Loss of consciousness due to an underlying cause

Answer 258

Cardiac Non cardiac Unknown Causes 1/3 idiopathic aetiology

Answer 259

Prodrome - hot and clammy - sweaty - heavy - dizzy or lightheaded - vision going blurry or dark - headache

Answer 260

Sit or lie down Have some water Have something to eat Wait till feel better

Answer 261

Examination ECG 24-hour ECG Echocardiograms Bloods

Answer 262

Reassurance + simple advice Avoid dehydration, missing meals, standing still for long periods of time.

Answer 263

Seizure Acute coronary syndrome Ventricular arrythmias Atrioventricular block Acute atrial fibrillation Congestive heart failure

Answer 264

Inflammation of the brain parenchyma associated with neurological dysfunction (altered state of consciousness or focal neurological signs).

Answer 265

Virus initially gains entry and replicates in local or regional tissue. Dissemination to the CNS occurs by haematogenous routes or via retrograde axonal transport

Answer 266

Result form antibodies directed against normal brain components Play a role in anti-N-methyl-D-aspartate receptor encephalitis and other paraneoplastic syndromes

Answer 267

Bimodal age pattern <1 and > 65 Seasonal and geographical variations - viral

Answer 268

Virus - Herpes virus - Ticks and mosquitos as vectors - HIV

Answer 269

Virus Bacterial Fungal Parasitic Para-infectious Prion diseases Paraneoplastic syndromes

Answer 270

Age <1 or > 65 Immunodefiency Post-infection Blood/body fluid exposures Organ transplantation Animal or insect bites Location Season Swimming or diving in warm freshwater

Answer 271

Often - mild flu like symptoms Can be more severe

Answer 272

Problems with speech and hearing Double vision Hallucinations Personality changes Loss of consciousness/sensation Muscle weakness Partial paralysis Impaired judgement Seizures Memory loss

Answer 273

Medical (+ neurological) exam + history Lab screening - blood, urine an bodily secretions Lumbar puncture Brain imaging

Answer 274

Antivirals - acyclovir and ganciclovir

Answer 275

Immunosuppressants Steroids

Answer 276

Specific for the cause Anticonvulsants Corticosteroids Artificial respiration Cognitive rehabilitation Physical speech Occupational therapy

Answer 277

Viral meningitis Encephalopathy - toxic/metabolic Status epilepticus CNS vasculitis Confusional migraine with pleocytosis Malignant hypertension

Answer 278

Hearing and/or speech loss Blindness Permeant brain and nerve damage Behavioural changes Cognitive disabilities Lack of muscle control Seizures Memory loss

Answer 279

May need long term therapy, medication and supportive care Mortality and morbidity vary depending on aetiology

Answer 280

Cryptococcus neoformans

Answer 281

All major fungal pathogens have capacity to cause meningitis Rapid aetiological diagnosis needed for antifungal therapy

Answer 282

HIV infection Corticosteroid use Underlying chronic disease Exposure to distributed soil, chicken guano or bat caves Neurosurgery

Answer 283

Lymphocytic pleocytosis Elevated protein Low glucose

Answer 284

Cloudy Protein - high Glucose - low High neutrophils Culture = bacterial

Answer 285

Clear Protein would be mildly raised or normal Glucose - normal High lymphocytes Culture - negative

Answer 286

Fungal blood cultures - 3 sets Serum cryptococcal antigen test Serum + urine histoplasma antigen

Answer 287

Aggressive therapy with antifungal agents Coccidoidal meningitis requires lifelong therapies

Answer 288

Poor prognosis with HIV-associated Mortality of non-HIV is associated with chronic renal failure, liver failure or haematological malignancy Mortality rates remain high

Answer 289

Autoimmune condition affecting the neuromuscular junction (similar to myasthenia gravis)

Answer 290

Antibodies against voltage-gated calcium channels Antibodies may be produced in response to small-cell lung cancer cells that express voltage-gated calcium channels Target and damage these channels in the presynaptic membrane of the neuromuscular junction = less Ach released into the synapse = weaker signal = reduced muscle contraction

Answer 291

50% paraneoplastic syndrome - small cell lung cancer Primary autoimmune disorder (usually autoimmune thyroid disease)

Answer 292

40% underlying cancer Median age onset 60s More frequent in males Underlying cancer = bimodal pattern Female < 45 yrs Male > 60 yrs

Answer 293

Proximal muscle weakness Autonomic dysfunction Reduced or absent tendon reflexes

Answer 294

Underlying small cell lung cancer or other malignancy Co-existing autoimmune disorder Cigarette smoking Family history of autoimmune disease

Answer 295

Lambert Eaton syndrome = reverse Reflexes may be absent in a rested patient but present when testing immediately after maximal muscle contraction

Answer 296

Nerve conduction studies Low frequency repetitive nerve stimulation Chest CT (cancer) Serology Thyroid-stimulating hormone

Answer 297

1st line - amifampridine

Answer 298

Exclude underlying malignancies Amifampridine Other options - pyridostigmine - immunosuppressants - IV immunoglobulins - Plasmapheresis

Answer 299

Botulism Myasthenia gravis Myopathy Chronic inflammatory demyelinating neuropathy Guillain-Barre syndrome

Answer 300

Osteoporosis Other corticosteroid-related adverse effects

Answer 301

Determined by presence and type of underlying cancer/autoimmune disease, the severity and distribution of weakness Weakness improves with cancer treatment

Answer 302

Meninges = meningioma Sellar region = craniopharyngioma Germ cell tumours Cranial nerves - schwannoma Hematopoietic - primary CNS lymphoma

Answer 303

Lung Breast Colorectal Testicular Renal cell Malignant melanoma

Answer 304

Tumour of glial cell - astrocytes/oligodendrocytes/ependymal cells

Answer 305

WHO grading system 1- 2 = low 3- 4 = high

Answer 306

Slow growing but will undergo anaplastic transformation

Answer 307

55% malignant 9th commonest cancer Commonest cause in men < 45, women < 35 Common differential diagnosis

Answer 308

Majority no cause Ionising radiation to the brain 5% family history Immunosuppression (CNS lymphoma)

Answer 309

Age Overweight and obesity Medical radiation - ionising radiation Family history

Answer 310

Headache Seizures Focal neurological symptoms Other non-focal symptoms - personality change/behaviour - memory disturbance - confusion

Answer 311

Papilledema Focal neurological deficit - hemiparesis - hemisensory loss - visual field defect - dysphasia

Answer 312

Woken by headache, worse in the morning and lying down Exacerbated by coughing, sneezing and drowsiness

Answer 313

Headache PLUS Aged > 50 New/changed headache Previous history of cancer

Answer 314

Typically present with seizures Can be incidental finding

Answer 315

Rapidly progressive neurological deficit Symptoms of raised intracranial pressure

Answer 316

CT - with contrast MRI - better for pituitary lesions Biopsy/surgery

Answer 317

No cure Steroids Surgery Radiotherapy Chemotherapy

Answer 318

6 months no treatment 18 months with

Answer 319

Surgery - early resection Radiotherapy Chemotherapy

Answer 320

Median survival 10 years

Answer 321

No - except grade 1

Answer 322

Brain metastasis Brain abscess Multiple sclerosis Necrosis Acute stroke Encephalitis

Answer 323

Features of raised intracranial pressure Other - new onset seizures - rapidly progressive focal neurology - past history of other cancer

Answer 324

Inherited disease that affects the peripheral and sensory neurones

Answer 325

Genetic mutations primarily affect the Schwann cell and myelin leads to demyelinating CMT Those affecting axons lead to axonal CMT

Answer 326

Autosomal dominant Autosomal recessive X-linked Heterogenous condition = most common

Answer 327

Family history

Answer 328

Symptoms start before the age of 10 Can be delayed until after 40

Answer 329

High foot arches - pev cavus Distal muscle wasting Lower leg weakness Weakness in the hands Reduced tendon reflexes Reduced muscle tone Peripheral sensory loss

Answer 330

Peripheral neuropathy Reduced sensory and motor function in peripheral nerves, typically affecting the feet and hands

Answer 331

Charcot Marie Tooth syndrome ABCDE Alcohol B12 deficiency Cancer and chronic kidney disease Diabetes and drugs Every vasculitis

Answer 332

Nerve conduction studies Genetic testing

Answer 333

No cure or treatment to stop from progressing Supportive management

Answer 334

Diabetes neuropathy Chronic inflammatory demyelinating polyneuropathy Acquired peripheral neuropathy Hereditary spastic paraplegia Spinocerebellar degeneration

Answer 335

Osteoarthritis Pain

Answer 336

Progressive condition Symptoms do not remit - worsen overtime No affective treatment or cure

Answer 337

Umbrella term for genetic conditions that cause gradual weakening and wasting of muscles

Answer 338

Duchenne Muscular Dystrophy

Answer 339

X-linked recessive condition

Answer 340

Defective gene for dystrophin on the X-chromosome Dystrophin = protein that helps hold muscles together on the cellular level Absence results in ongoing cell membrane depolarisation Degeneration is faster than regeneration - muscle fibres undergo necrosis Muscle fibres are replaced by adipose and connective tissue = muscle progressively weaken

Answer 341

Family history Male sex

Answer 342

Boys Present at 3-5 years Weakness in the muscles around their pelvis Weakness = progressive, eventually all muscles will be affected

Answer 343

Delayed motor milestones Frequent falls Abnormal gait Muscle Pain Calf hypertrophy Speech and language delay Difficulty jumping, running, climbing steps and rising from the floor

Answer 344

Serum creatinine kinase Genetic testing (Xp21 mutation) Gower's sign

Answer 345

Shows proximal muscle weakness To stand up from lying position will have to get onto hands and knees, push their hips and backwards like a downward dog pose

Answer 346

Genetic testing

Answer 347

Oral steroids Creatinine supplementation Genetic trials Supportive treatment

Answer 348

Allowing the person to have highest quality of life for the longest time possible

Answer 349

Other muscular dystrophies Polymyositis Static encephalopathies - cerebral palsy

Answer 350

Most patients lose ability to walk at 12 years Require ventilation support by 20 Life expectancy 25-35 years - due to cardiac and respiratory complications

Answer 351

Respiratory failure Loss of mobility Osteoporosis Weight loss/malnutrition Sexual dysfunction Impaired growth Delayed puberty Constipation

Answer 352

Occurs due to damage to one lateral side of the spinal cord and most commonly occurs in the cervical region Incomplete spinal injury

Answer 353

Partial hemi section Often includes the nerve tracts lying along the path of the injured area involved

Answer 354

Trauma Tumour Inadequate or blocked blood flow through a blood vessel to part of the body Infectious disease e.g. TB Inflammatory disease e.g. multiple sclerosis

Answer 355

Ipsilateral spastic paralysis below the level of the lesion Ipsilateral loss of fine touch, proprioception and vibration sense Contralateral loss of pain and temperature sensation

Answer 356

DCML pathway

Answer 357

Anterolateral system

Answer 358

Detailed history Examination Lab tests Diagnostic testing - MRI

Answer 359

High-dose steroids

Answer 360

High dose steroids Perioperative prophylactic antibiotics Address underlying cause

Answer 361

Stroke Tumour or cysts Spinal infection Spinal cord tumour, primary or metastatic Spinal cord herniation

Answer 362

Varies on cause Potential for significant recovery is strong (50%) Take up to 2 years for neurological recovery

Answer 363

Hypotension or spinal shock Depression Pulmonary embolism Infections - UTI, lungs

Answer 364

Special visceral afferent fibres for the sense of smell Passes through the cribriform plate of the skull

Answer 365

Trauma, tumour Decreased ability to smell

Answer 366

Special somatic afferent fibres for vision Afferent limb for pupillary light reflex Passes through the optic canal of the skull

Answer 367

Trauma, tumour (pituitary adenomas and craniopharyngioma), MS, stroke Blindness, visual field defect

Answer 368

General somatic efferent and general visceral efferent fibres to the extraocular muscles and pupillary constrictor muscles Efferent limb for the pupillary light reflex

Answer 369

Levator palpebrae superiors Inferior oblique Superior, medial and inferior recti

Answer 370

Passes through the superior orbital fissure of the skull

Answer 371

Diabetes, increased intra-cranial pressure CN III causes a 'down and out' eye Dilated pupils Ptosis

Answer 372

Provides general somatic efferent to the extraocular superior oblique muscles Depresses and abducts the eye Passes through the superior orbital fissure.

Answer 373

Trauma Diplopia

Answer 374

3 sensory nuclei 1. Mesencephalic - proprioception 2. Principal - light touch and discrimination 3. Spinal - pain and temperature, crude touch

Answer 375

Sensory - idiopathic, trauma, inguinal nerve damage Motor - bulbar palsy No signs - sensory deficit on testing May have decreased facial sensation

Answer 376

General somatic afferent to above the lower eyelid

Answer 377

General somatic afferent of the lower eyelid to the upper lip

Answer 378

General somatic afferent and special visceral efferent to below the upper lip

Answer 379

General somatic efferent fibres for eye abduction Innervates the lateral rectus muscle Passes through the superior orbital fissure of the skull

Answer 380

MS, some strokes Inability of the eye to look laterally Eye deviated towards the nose

Answer 381

General somatic afferent - skin behind the ear Special visceral afferent - taste to anterior 2/3 of the tongue General visceral efferent - parasympathetic to the lacrimal, subinguinal and submandibular gland Special visceral efferent - muscles of facial expression

Answer 382

LMN - Bell's palsy, skull fracture, parotid tumour = total facial weakness UMN - stroke, tumour = forehead sparing weakness

Answer 383

Provide special somatic afferent = hearing and balance Does not leave the skull Cochlea = sound waves to mechanical ossicle movements Vestibular apparats = detect changes in head motion

Answer 384

Excess noise, Paget's, acoustic neuroma Deafness

Answer 385

General somatic afferent = sensation from the posterior Special visceral afferent = taste to posterior 1/3 of the tongue General visceral efferent = parasympathetic to parotid glands Special visceral efferent = motor to stylopharyngeus

Answer 386

Trauma, tumour Impaired gag reflex

Answer 387

General somatic afferent = skin around the ear Special visceral afferent = taste and sensation to the epiglottis General visceral afferent = sensory information to body viscera General visceral efferent = parasympathetic to glands of GI tract Special visceral efferent = motor innervation to soft palate, pharynx and larynx

Answer 388

Trauma, brainstem lesions Impaired gag reflex, soft palate moves 'good' side on saying 'ahh'

Answer 389

General somatic efferent fibres to the trapezius and sternocleidomastoid

Answer 390

Polio, stroke Weakness turning the head away from the affected side (sternocleidomastoid) Weakness shrugging shoulders (trapezius)

Answer 391

General somatic efferent fibres for controlling tongue muscles

Answer 392

Trauma, brainstem lesions Tongue deviated to affected side on protrusion

Answer 393

Compression of the medial nerve as it travels through the carpal tunnel in the wrist. Causes pain and numbness in the median nerve distribution on the hand.

Answer 394

Either: Swelling of the contents - swelling of the tendon sheaths due to repetitive strain Narrowing of the tunnel

Answer 395

Abductor pollicis brevis - thumb abduction Opponens pollicis - thumb opposition Flexor pollicis brevis - thumb flexion

Answer 396

Sensory innervation of the palmar aspects and full fingertips of the: Thumb Index and middle finger The lateral half of the ring finger

Answer 397

Females between 40-60 years

Answer 398

No clear cause found Idiopathic

Answer 399

Repetitive strain Obesity Perimenopause Rheumatoid arthiritis Diabetes Acromegaly Hypothyroidism

Answer 400

Gradual onset - start intermittent Worse at night time

Answer 401

Palmar digital cutaneous branch of the median nerve - Numbness - paraesthesia - Burning sensation - Pain

Answer 402

To thenar muscles - weakness of thumb movements - weakness of grip strength - difficulty with fine movements involving the thumb - Wasting of the thenar muscle - atrophy

Answer 403

Phalen's test Tinel's test

Answer 404

Full flexing and holding it in its position Test positive = position submandibular sensory symptoms of the carpal tunnel

Answer 405

Tapping the wrist at the location where the median nerve travels through the carpal tunnel Positive = triggers sensory symptoms of carpal tunnel

Answer 406

Electromyogram (EMG)

Answer 407

Wrist splint Corticosteroid injection Surgical release

Answer 408

Osteoarthritis Stroke Ulnar neuropathy MND De Quervain's tenosynovitis

Answer 409

Radial nerve damage leading to weakness in the wrist and fingers

Answer 410

Radial nerve exists the upper spinal cord, travels down the upper arm very close to humerus. Gives off several branches. May be damaged at the level of the humerus or in the elbow/forearm

Answer 411

Named 'Saturday night palsy' Aged between 75-84

Answer 412

Humerus (upper arm) Forearm

Answer 413

Fracture Sitting or sleeping with arm over back of chair Repetitive use Injuries - stab wombs Lead poisoning and thiamine deficiency Limb onset ALS Acute upper limb ischemia

Answer 414

Weak wrist/fingers/thumb Close to origin = weak elbow Numbness or tingling present over the back of the thumb

Answer 415

Nerve conduction and needle electromyography Plain x-ray MRI High resolution ultrasound

Answer 416

Usually recover without treatment - weeks or months Possible - wrist splint - physical therapy - possible surgery

Answer 417

Posterior interosseous neuropathy Posterior cord Radial neuropathy in the spinal groove/axilla

Answer 418

Deformity with hyperextension of the MCP joints and flexion of the IPJ due to weakness of the intrinsic muscles of the hand

Answer 419

Complete - involves all digits - results from both ulnar and median palsy Incomplete/partial - involves only ulnar 2 digits - referred to as isolated ulnar nerve palsy

Answer 420

Nerve damage in the arm Congenital birth defect Some genetic diseases e.g. Charcot-Marie Tooth Disease Bacterial infections e.g. leprosy Scarring after a severe hand or forearm burn Compartment syndrome of the hand

Answer 421

External compression at the elbow Body weight pressure onto tools Prolong movements causing the elbow to lean e.g. cyclists, desk jobs

Answer 422

Muscle wasting on the interosseous and hypothenar Numbness along the nerve involved Inability to extend the IP joints during extension of the fingers - abduct and adduct fingers Unopposed action of the extensor and the flexor digitorum profundus.

Answer 423

Electromyography Nerve conduction studies

Answer 424

Splinting Surgery Tendon transfer (graft) Therapy to straighten fingers Physiotherapy management

Answer 425

Cervical radiculopathy Dypuytren contracture Klumpke's paralysis Lower brachial plexopathy

Answer 426

Not a disease Symptom of neurological, anatomical or muscular problem. Inability to lift the forefoot due to the weakness of dorsiflexors of the foot

Answer 427

Damage to the common peroneal nerve - weakness of tibialis anterior and other key dorsiflexors of the foot

Answer 428

Compression disorders Traumatic injuries Neurological disorders

Answer 429

Fibular nerve compression Sciatic nerve compression Lumbar disc herniation or spondylitis of the spine

Answer 430

Charcot-Marie Tooth Stroke

Answer 431

No active dorsiflexion in a non-weight bearing position Gait assessment Pain - Neurogenic pain - Sensory changes

Answer 432

Gait assessment History Assessment of ankle dorsiflexion Neurological exam Electromyography/nerve conduction studies

Answer 433

2/3 resolve within 1 year Analgesia Splinting Physiotherapy - exercise Surgery

Answer 434

L5 radicopathy UMN lesion Chronic/persistent pain Sciatic nerve injury

Answer 435

Sciatica Spinal stenosis

Answer 436

Narrowing of part of the spinal canal, resulting in compression of the spinal cord or nerve roots typically resulting from degenerative changes in the lumbar spine

Answer 437

Degenerative disease of lumbar spine may reduce the diameter of the spinal canal May produce narrowing of the lateral recess and neural foramina Stenosis results from a cascade of micro-degenerative changes

Answer 438

Central stenosis - narrowing of the central spinal canal Lateral stenosis - narrowing of the nerve root canals Foramina stenosis - narrowing of the intervertebral foramina

Answer 439

> 60 - degenerative changes

Answer 440

Congenital spinal stenosis Degenerative changes Herniated discs Thickening of the ligamenta flava or posterior longitudinal ligament Spinal fractures Spondylolisthesis Tumours

Answer 441

Age > 40 Previous back surgery Previous injury Achondroplasia Acromegaly

Answer 442

Gradual onset Severity of symptoms will depend on the degree of narrowing and spinal cord compression

Answer 443

Symptoms of cauda equina syndrome - Saddle anaesthesia - sexual dysfunction - incontinence of bladder and bowel Requires emergency management

Answer 444

Intermittent neurogenic claudication of lumbar spine stenosis with central stenosis - Lower back pain - Buttock and leg pain - Leg weakness

Answer 445

Compression of the nerve roots as they exit the spinal cord and spinal column - leads to motor and sensory symptoms

Answer 446

MRI Other - angiogram

Answer 447

NSAIDs + physiotherapy

Answer 448

1st line - NSAIDs + physiotherapy Epidural corticosteroid injections Decompressive spinal surgery Laminectomy

Answer 449

Peripheral vascular disease Lumbosacral intervertebral disc herniation Spinal compression fracture Metastatic disease of spine Ankylosing spondylitis

Answer 450

Supplies sensation to the lateral lower leg and the foot Motor function to the posterior thigh, lower leg and foot

Answer 451

Symptoms associated with irritation of the sciatic nerve

Answer 452

Due to lumbosacral nerve root compression Herniated disc Spondylolisthesis Spinal stenosis

Answer 453

Unilateral pain from buttock radiating down the back of the thigh to below the knee or feet Paraesthesia Numbness Motor weakness Reflexes may be affected

Answer 454

Amitriptyline Duloxetine NO opioids

Answer 455

Either: Ischaemic stroke Intracranial haemorrhage

Answer 456

Ischemia (inadequate blood supply) or infarction (tissue death due to ischemia) of the brain secondary to a disrupted blood supply Blood supply in a cerebral vascular territory is critically reduced due to occlusion or critical stenosis of a cerebral artery

Answer 457

Bleeding in or around the brain

Answer 458

Involves temporary neurological dysfunction (lasting less than 24 hours) caused by ischaemia but without infarction

Answer 459

2 or more TIAs within a week and indicate a high risk of stroke

Answer 460

Cerebral blood flow falls - brain compensates by increasing oxygen extraction Partial blood flow = neuronal function is impaired. Cell death is delayed by minutes to hours Restoration of flow via autolysis of occluding thrombus, can arrest the progression to infarction

Answer 461

Caused by transient or permeant critical reduction in cerebral blood flow due to arterial occlusion or stenosis Thrombus or embolus Atherosclerosis Shock Vasculitis

Answer 462

In situ thrombosis of an intracranial artery or artery-to-artery embolism of thrombus as a result of stenosis or unstable atherosclerotic plaque Occlusion due to - hypercoagulability - dissection - vasculitis - vasospasm - sickle cell occlusive disease

Answer 463

Previous history AF Carotid artery stenosis Hypertension Diabetes Raised cholesterol Family history Smoking Obesity Vasculitis Combined contraceptive pill

Answer 464

Sudden onset of neurological features Asymmetrical Limb/facial weakness Dysphasia Visual field defect Sensory loss Ataxia and vertigo

Answer 465

For a stroke Face Arm Speech Time - act fast and call 999

Answer 466

ROSIER tool

Answer 467

Recognition of a stroke Gives a score based on clinical features and duration Stroke possible in patients scoring 1 or more

Answer 468

Diffusion weighted MRI

Answer 469

Non-contrast CT

Answer 470

Symptoms usually resolve within 24 hours of onset Initial - Aspirin - Referral for specialised assessment - MRI Assessment of underlying cause

Answer 471

Exclude hypoglycaemia Immediate CT brain (exclude haemorrhage) Aspirin Admission

Answer 472

Thrombolysis with alteplase Thrombectomy

Answer 473

With alteplase - tissue plasminogen activation that rapidly breaks down clots Given 4.5 hours within symptom onset Close monitoring for complications

Answer 474

Blockage of the proximal anterior circulation or proximal posterior circulation Within 24 hours of the symptom onset Alongside IV thrombolysis

Answer 475

Lowering blood pressure can worsen the ischemia High blood pressure treatment only indicated in hypertensive emergency or reduce risks when giving IV thrombolysis

Answer 476

Aggressively treated

Answer 477

Ischemic/haemorrhagic TIA Hypoglycaemia Complicated migraine Wernicke's encephalopathy

Answer 478

Clopidogrel Atorvastatin Blood pressure and diabetes control Addressing risk factors

Answer 479

Aspiration Pneumonia Depression DVT

Answer 480

Risk of recurrent stroke is high in the first 7 days following a TIA

Answer 481

Caused by vascular rupture into the brain parenchyma Results in primary mechanical injury to the brain tissue. Expanding haematoma may shear additional neighbouring arteries Results in secondary ischemic injury

Answer 482

Head injuries Ischemic stroke Aneurysms Ischemic stroke - progressing to bleeding Brain tumours Thrombocytopenia Bleeding disorders Anticoagulants

Answer 483

Key feature = sudden-onset headache Seizures Vomiting Reduced consciousness Focal neurological symptoms

Answer 484

Immediate CT head Bloods - FBC - Coagulation screen

Answer 485

Glasgow Coma Score

Answer 486

Score based on eyes, verbal response and motor response Maximum score 15/15 8/15 needs airway support

Answer 487

Correct clotting abnormality Small bleeds - manage conservatively Extradural or subdural - craniotomy - Burr holes

Answer 488

Ischaemic stroke Hypertensive encephalopathy Hypoglycaemia Complicated migraine Seizure disorder

Answer 489

Between the skull and dura mater

Answer 490

Rupture of the middle meningeal artery in the temporoparietal region Associated with a fracture of the temporal bone

Answer 491

Young patient Traumatic head injury Ongoing headache Period of improved neurological symptoms and consciousness Followed by rapid decline over hours as the haematoma gets large enough to compress the intracranial contents

Answer 492

CT scan - Bi-convex shape - limited by cranial sutures

Answer 493

Occurs between the dura and arachnoid mater

Answer 494

Elderly and alcoholic patients - more atrophy in the brains = vessels more prone to rupture

Answer 495

Rupture of the bridging veins in the outermost meningeal layer

Answer 496

CT - Crescent shape - not limited to cranial sutures

Answer 497

Involves bleeding in the brain tissue

Answer 498

Lobar Deep Intraventricular Basal ganglia Cerebellar

Answer 499

Occur spontaneously OR Secondary to ischemic stroke, tumours, or aneurysm stroke

Answer 500

Presents like an ischemic stroke Sudden onset focal neurological symptoms - limb weakness - dysphasia - vision loss

Answer 501

Bleeding in the subarachnoid space when the CSF is located - between the pia mater and the arachnoid membrane

Answer 502

Ruptured cerebral aneurysm

Answer 503

Sudden onset occipital headache during strenuous activity Sudden or severe onset - leads to thunderclap headache description

Answer 504

Epileptic seizures Syncope (vasovagal) Postural (orthostatic) hypotension Hypoglycaemia Non-epileptic attack disorder

Answer 505

Prodromal aura Conclusive jerk Eyes open Automatism, lateral tongue biting Cyanotic/pale Post-ictal confusion Long recovery period

Answer 506

Epileptic seizure

Answer 507

Trigger e.g. blood, standing, needles Prodrome - nausea, light-headiness, pallor Incontinence may feature Brief convulsive jerks

Answer 508

Syncope (vasovagal)

Answer 509

Features/history of arrythmias/structural abnormalities

Answer 510

Cardiac syncope

Answer 511

Use of vasodilators, antidepressants

Answer 512

Postural (orthostatic) hypotension

Answer 513

Features of adrenaline release - palpitations, sweating, agitation

Answer 514

Hypoglycaemia

Answer 515

Normal colour Eye closed with active resistance to opening Retained consciousness, combative Pelvic thrust, arching back, erratic mvt

Answer 516

Non-epileptic attack disorder

Answer 517

6 questions

Answer 518

MOCA - Montreal cognitive assessment MMSE - mini-mental state examination

Answer 519

23 or lower indicates dementia

Answer 520

Hearing Language compression Sematic knowledge Memory Emotional/affective disorder behaviour Amnesic

Answer 521

Failure to create new memories.

Answer 522

Stop smoking Body mass index - 18-25 kg/m2 Diet - consumption of 3+ fruit/vegetables + < 30% of calories from fat Physical activity - 2+ miles walk or 10+ cycling, vigorous exercise Alcohol < 3 units per day

Answer 523

Acetyl choline esterase inhibitors (cholinesterase inhibitors) Slows down progression

Answer 524

To dye blood vessels

Answer 525

Subarachnoid headache

Answer 526

Unilateral

Answer 527

Spinal cord compression Cauda equina Pathological fractures Prolapse disk Metastasis Multiple sclerosis MRI

Answer 528

Multiple sclerosis

Answer 529

High dose steroids - prednisolone

Answer 530

Riluzole Sodium channel blocker which inhibits glutamate release

Answer 531

Blood glucose - hypoglycaemia ECG - heart conditions

Answer 532

Sodium valproate

Answer 533

Nerve conduction studies

Answer 534

Globe depressed and abducted Fixed dilated pupil

Answer 535

Ipsilateral side - Horner's syndrome - limb ataxia - loss of facial sensation of pain, temp on face, reduced corneal reflex. - dysarthria - dysphagia Contralateral side - loss of pain and temp sensation

Answer 536

Lesion of sympathetic chain supplying the eye

Answer 537

Dilator pupillae - involved in mydriasis or dilation of the pupil Superior tarsal muscle - aids in elevating the upper eyelid with levator palpebrae superioris Sweat glands

Answer 538

Localising or pressure related

Answer 539

Describes the relationship between the contents of the cranium and intracranial pressure. 3 components - CSF volume (150ml 10%) - Blood volume (150ml 10%) - Brain parenchyma volume (1400ml 80%)

Answer 540

= Pressure within the cranium of the skull. Cranium is fixed, increase in volume of one of the other intracranial components will result in increased pressure. Equilibrium between these components

Answer 541

MRI head with contrast (gadolinium) +/- spine

Answer 542

Ring enhancement around the outer edge of the tumour Differentials - abscesses

Answer 543

Periventricular - around the tumour Steroids can cause temporary shrinking - can make biopsy difficult

Answer 544

Brainstem motor nuclei Cranial nerve Neuromuscular junction Muscle

Answer 545

Motor cortex Corticobulbar tract

Answer 546

LMN problem affecting bilateral IX, X, XI and XIII (at the level of the brainstem nuclei, nerve fascicles or lower cranial nerves outside the brainstem

Answer 547

UMN problem occurring above the level of the brainstem nuclei e.g. affecting bilateral corticobulbar tracts (also associated with emotional lability)

Answer 548

Absent Absent Wasting and fasciculations Nasal LMN signs

Answer 549

Absent Increased Spastic, hard to protrude Spastic dysarthria - 'hot potato speech' UMN signs Emotional labiality, brisk jaw jerk

Answer 550

Difficulty speaking because the muscles used to speak are weak

Answer 551

Having difficulty making sounds when attempting to speak

Answer 552

Language disorder that affects the ability to produce and understand spoken language

Answer 553

Difficulty expressing what you want to say

Answer 554

Difficulty understanding the speech of others

Answer 555

Pyridostigmine Long acting acetylcholinesterase

The Brain Flashcards

(587 cards)