Neurology Flashcards

1
Q

Pathological basis of meningitis

A

Inflammation of the pia and arachnoid mater
Microorganisms infect the CSF
Not always an infective cause e.g. can be post surgical

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2
Q

Symptoms of meningitis

A

TRIAD: Stiffness of the neck, Severe headache, and Fever (infective)
Photophobia
Meningococcal meningitis: petechial non blanching rash

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3
Q

Two most common bacterial causes of meningitis in adults

A
Diplococcus bacteria: 
Neisseria Meningitidis (meningococcal meningitis) -ve (non-blanching rash) 
Streptococcus Pneumoniae (pneumococcal meningitis) +ve
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4
Q

Viral causes of meningitis

A

Mumps virus
Coxsackie virus
HSV

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5
Q

Drug induced meningitis

A

NSAIDs

Trimethoprim

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6
Q

Diagnosis of meningitis

A

Blood culture

Brain imaging

CSF sample (lumbar puncture at L4) for microscopy and sensitivity testing

  • bacteria: turpid yellow colour, neutrophil polymorphs, raised protein, low glucose
  • viral: lymphocytes, normal protein, normal glucose
  • TB: lymphocytes, raised protein, low/normal glucose

PCR swab for viral

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7
Q

Treatment for bacterial meningitis

A

If suspected, give broad spectrum antibiotics before tests come back

Cephalosporins: IV ceftriaxone/IV cefotaxime

Over 50/immunocompromised: add IV amoxicillin

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8
Q

Treatment for viral meningitis

A

Supportive treatment
Self-limiting in 4-10 days
Acyclovir for HSV meningitis

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9
Q

Types of STROKE

A

Cerebral infarction (ischaemic stroke)
Intracerebral haemorrhage
Subarachnoid haemorrhage

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10
Q

Transient ischaemic attack Px

A

SUDDEN ONSET
Brief episode of neurological deficit
Symptoms are maximal at onset (usually last 5-15 mins)
LASTS <24 HOURS
WITHOUT INFARCTION (temporary, focal cerebral ischaemia)

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11
Q

TIA epidemiology

A

MALES

African-Caribbean heritage (HTN and atherosclerosis)

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12
Q

TIA and ischaemic stroke RFs

A
Age
HTN
Smoking
Diabetes
Combined pill
Atrial fibrillation 
Male
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13
Q

Causes of a TIA

A

Atherothromboembolism
- carotid artery = main cause (carotid bruit)

Cardioembolism

  • atrial fibrillation
  • post-MI
  • valve disease/prosthetic

Hyperviscosity

Hypoperfusion

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14
Q

DDx TIA

A
Hypoglycaemia
Migraine aura
Focal epilepsy
Vasculitis 
Syncope
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15
Q

Clinical presentation of a TIA (carotid territory Sx - 90%)

A
Amaurosis fugax
Aphasia
Hemiparesis
Hemisensory loss
Hemianopic visual loss
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16
Q

Amaurosis fugax

A

Temporary occlusion of retinal artery (temporary retinal hypoxia)

Unilateral sudden vision loss

Transient (minutes)

“like a curtain descending”

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17
Q

ABCD2 score

A

Risk of stroke after TIA

Age
Blood pressure
Clinical features (unilateral weakness, speech disturbance w/o weakness)
Duration (<60 mins = 1, >60 mins = 2) 
Diabetes mellitus
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18
Q

Ix for TIA

A

CLINICAL DIAGNOSIS based off symptoms description

Bloods: glucose, FBC (polycythaemia), ESR (vasculitis), U&Es, cholesterol, INR (if on warfarin)

Imaging: diffusion weighted MRI or CT

Carotid imaging: doppler ultrasound, MR/CT angiography if stenosis

ECG

Echocardiogram

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19
Q

IMMEDIATE Mx for TIA

A

Aspirin 300mg

Refer to specialist (within 24h of symptom onset)

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20
Q

Long term Mx of TIA

A

Control CV risk factors

  • BP control
  • Smoking cessation
  • Statin e.g. simvastatin
  • No driving (1 month)

Antiplatelet therapy: CLOPIDOGREL

AF: anticoagulation (e.g. warfarin)

> 70% carotid stenosis: carotid endartectomy (reduces stroke risk by 75%)

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21
Q

Stroke

A

rapid onset neurological deficit lasting for over 24 hours

poor blood flow to the brain causes cell death

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22
Q

Two types of stroke

A

Ischaemic (85%)
Haemorrhagic (15%)
1st line Ix: CT HEAD

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23
Q

Penumbra

A

Infarcted area in ischaemic stroke is surrounded by a swollen area (oedema) which can regain function with neurological recovery

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24
Q

Causes of ischaemic stroke

A

Small vessel occlusion by thrombus

Atherothromboembolism (e.g. from carotid artery)

Cardioembolism (AF, post-MI, valve disease, IE)

Hyperviscosity
Vasculitis
Hypoperfusion

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25
Clinical Px of ischaemic stroke (cerebral infarct)
Depends on the site (ACA, MCA, PCA) ``` Contralateral sensory loss Contralateral hemiplegia: initially flaccid, becomes spastic (UMN lesion) UMN facial weakness (forehead sparing) Dysphasia Homonymous hemianopia Visuo-spatial deficit ``` Weakness may recover gradually
26
Human homunculus blood supply
ACA (medial supply): lower limbs MCA (lateral supply): face, upper limbs
27
Clinical Px of ischaemic stroke (brainstem infarct)
``` Quadriplegia Locked-in syndrome Facial numbness and paralysis Vision disturbances Vertigo, nausea Cerebellar signs ```
28
Lacunar infarct
``` Small infarcts Occur in single small perforating artery supplying a subcortical area - Internal capsule - Basal ganglia - Thalamus - Pons ``` Px one of: sensory loss, weakness (unilateral), ataxic hemiparesis, dysarthria (motor speech)
29
Ischaemic stroke and intracerebral haemorrhage Ix
CT scan - distinguish ischaemic from haemorrhagic - site of infarct - identify mimics Diffusion-weighted MRI: - more sensitive - CT may be -ve in first few hours - unclear diagnosis Bloods: glucose (rule out hypoglycaemia), FBC (polycythaemia), ESR (vasculitis), U&Es, Cholesterol, INR (warfarin) ECG: AF, MI
30
Immediate ischaemic stroke Mx
EXCLUDE HAEMORRHAGE loading dose: Aspirin 300mg Admit to acute stroke unit Thrombolysis (must happen within 4.5 hours of symptom onset for risk/benefit ratio) - IV alteplase - MANY contraindications
31
Long term ischaemic stroke Mx
Aspirin 300mg for 2 weeks Clopidogrel daily long term Anticoagulation (e.g. warfarin) for patients with AF Rehabilitation
32
Intracerebral haemorrhage epidemiology
around 10% of strokes | higher mortality: up to 50%
33
Pathophysiology of increased ICP in an intracerebral haemorrhage
Pooling blood puts pressure on skull, brain & blood vessels - healthy tissue can die CSF obstruction - hydrocephalus Midline shift Tentorial herniation Coning (compression of the brainstem)
34
Intracerebral haemorrhage RFs
HYPERTENSION Anticoagulation Thrombolysis Age, Alcohol, Smoking, Diabetes
35
Two causes of intracerebral haemorrhage
HYPERTENSION: stiff and brittle vessels are prone to rupture + microaneurysms SECONDARY to ischaemic stroke (bleeding after reperfusion)
36
Clinical presentation of intracerebral haemorrhage
- similar to ischaemic stroke - ``` Pointers to haemorrhage: SUDDEN LOSS of consciousness SEVERE HEADACHE MENINGISM COMA ```
37
Intracerebral haemorrhage Tx
Stop anticoagulants immediately Control BP Reduce ICP - mechanical ventilation - IV MANNITOL Neurosurgical evaluation if: - hydrocephalus - coma - brainstem compression
38
Vessels in subarachnoid space
circle of willis arteries
39
Vessels in subdural space
bridging veins (drain from cortex into dural venous sinus > IJV)
40
Vessels in extradural space
middle meningeal artery
41
most common type of brain aneurysm
``` berry aneurysm (90%) - bursting most commonly results in SUBARACHNOID (70-80% of SAH cases) at circle of willis (ACA, MCA, PCA) ```
42
SAH typical age
35-65
43
RFs associated with berry aneurysms
Polycystic kidney disease Coarctation of aorta Connective tissue disorders
44
SAH RFs
``` Hypertension Known aneurysm Previous aneurysmal SAH Berry aneurysm RF e.g. PKD Smoking, alcohol ```
45
Berry aneurysms make up 70-80% of SAH cases, what are the other causes?
Traumatic injury ARTERIOVENOUS MALFORMATIONS (15%): abnormal tangle of blood vessels connecting arteries and veins IDIOPATHIC (15-20%)
46
Complications of SAH
Rebleeding | Hyponatraemia
47
SAH pathophysiology
Tissue ischaemia - less blood to reach tissue > less O2 + nutrients > cell death Raised ICP Space-occupying lesion (puts pressure on brain) Meningism - blood irritates meninges - can obstruct CSF outflow (hydrocephalus) Vasospasm - bleeding irritates other vessels - ischaemic injury
48
SAH symptoms
SUDDEN ONSET EXCRUCIATING HEADACHE - "Thunderclap" "worst ever headache" - Typically OCCIPITAL Nausea, vomiting, collapse, loss of consciousness Seizures, vision changes, coma Mild photophobia/neck stiffness Sentinel headache before main rupture in some cases
49
SAH signs
Meningeal irritation: - Neck stiffness - Kernig's sign - Brudzinski's sign Retinal bleed -/+ papilloedema (worse prognosis) Focal neurological signs e.g. 3rd nerve palsy Increased BP
50
DDx in SAH
Headache - MIGRAINE - Cluster headache MENINGITIS Intracerebral haemorrhage
51
CT scan in SAH
ASAP Detects >95% of SAH in first 24 hours Findings of subarachnoid or intraventricular blood "Star" shaped sign
52
Lumbar puncture in SAH
Only do a lumbar puncture if NORMAL ICP (to prevent CONING) Indication: if -ve CT but strong suspicion of SAH remains - after 12 hours Finding: XANTHOCHROMIA (yellowish CSF with RBC breakdown products e.g. bilirubin)
53
Mx in SAH
Immediately refer to neurosurgeon IV fluids (maintain cerebral perfusion) Hydrocephalus: ventricular drainage NIMODIPINE: calcium antagonist, reduces vasospasm (reducing ischaemic risk) Surgery: if angiography has shown aneurysm, endovascular coiling
54
Main cause of subdural haematoma
Head trauma
55
Px SDH
MASSIVE LATENT INTERVAL (weeks to months) [often cannot remember the traumatic injury as it was so long ago] Symptoms: fluctuating level of consciousness, drowsiness, headache, confusion Signs: raised ICP, seizures, neurological signs (hemiparesis, unequal pupils)
56
SDH epidemiology + risk factors
BABIES: "shaking baby syndrome" traumatic injury DEMENTIA, ELDERLY, ALCOHOLICS - BRAIN ATROPHY (veins are more susceptible to rupture) - more accident-prone (risk of falls) + epileptics Anticoagulation
57
Ix SDH
CT: - CRESCENT SHAPED (BANANA) - Unilateral - MIDLINE SHIFT
58
Subdural haemotoma pathophysiology
Bridging vein bleeding > haemotoma > bleeding stops > weeks/months later = haemotoma AUTOLYSES = massive increase in ONCOTIC and OSMOSTIC pressure = WATER SUCKED IN = haemotoma enlarges Gradual rise in ICP over WEEKS Midline structures shifted away from side of clot = tentorial herniation + coning
59
Ix SDH
``` CT: Haematoma: - CRESCENT SHAPED (BANANA) - Unilateral - MIDLINE SHIFT ``` MRI scan
60
Mx SDH
SURGERY depends on clot SIZE, CHRONICITY, CLINICAL PICTURE - clot evacuation - craniotomy IV MANNITOL (reduce ICP) Reverse clotting abnormalities Address cause of trauma (falls, abuse)
61
EDH epidemiology
mostly in YOUNG PEOPLE more common in MALES
62
EDH pathophysiology
After LUCID INTERVAL: - rapid rise in ICP - midline shift - tentorial herniation - coning
63
EDH clinical Px
``` Lucid interval Rapidly declining GCS (consciousness level) Increasingly severe headache Vomiting Seizures ```
64
EDH Ix
CT: - LENS SHAPED (LEMON) - Doesn't cross suture lines (trapped in skull) - Unilateral - Midline shift Skull X-Ray: fractures
65
EDH clinical Px
``` Lucid interval RAPIDLY DECLINING GCS (consciousness level) Increasingly severe HEADACHE VOMITING SEIZURES Hemiparesis UMN signs COMA Deep and irregular breathing (due to coning) DEATH (respiratory arrest) ```
66
EDH Ix
``` CT: Haematoma: - LENS SHAPED (LEMON) - DOESN'T cross suture lines (trapped in skull) - Unilateral - Midline shift ``` Skull X-Ray: fractures
67
What is a migraine?
RECURRENT throbbing UNILATERAL headache often preceded by an AURA and associated NAUSEA, VOMITING, and VISUAL CHANGES
68
Most common cause of episodic headaches
Migraines
69
Migraines epidemiology
90% onset before 40 years | More common in females (roughly 3x)
70
Migraines RFs
Genetics (FHx) Female Age (majority of first ones occur in adolescence)
71
Migraine triggers
``` CHOCOLATE Chocolate Hangovers Orgasms Cheese Oral contraceptives Lie-ins Alcohol Tumult i.e. loud noises Exercise ```
72
Migraine prodrome
yawning, cravings, mood/sleep changes
73
Aura
precedes migraine attack variety of symptoms: visual disturbance e.g. lines, dots, zig-zags somatosensory e.g. parasthesia, pins & needles migraines can be classified WITH or WITHOUT AURA
74
Aura preceding migraine attack
variety of symptoms: visual disturbance e.g. lines, dots, zig-zags somatosensory e.g. parasthesia, pins & needles migraines can be classified WITH or WITHOUT AURA
75
Migraine diagnostic criteria
``` ATLEAST 2 OF: Unilateral pain (usually 4-72 hours) Throbbing-type pain Moderate-severe intensity Motion sensitivity ``` PLUS, AT LEAST 1 OF: Nausea/vomiting Photophobia/phonophobia ALSO: NORMAL EXAMINATION & NO ATTRIBUTABLE CAUSE
76
Migraine Ix
Clinical diagnosis with few or no Ix required Certain cases may require rule outs e.g. blood tests, CT/MRI, lumbar puncture
77
Migraine red flag indications for CT/MRI
``` Thunderclap headache Change in pattern Abnormal neuro exam Onset > 50 years Epilepsy Posteriorly located headache ```
78
Migraine treatment
1st line acute = ORAL TRIPTANS E.G. SUMATRIPTAN - c/i in IHD + uncontrolled HTN - s/e: arrhythmias, angina NSAIDs e.g. naproxen Anti-emetics e.g. prochlorperazine AVOID OPIOIDS & ERGOTAMINE
79
Migraine PROPHYLAXIS
Required if >2 attacks per month OR if acute meds are required >2 per week Triad: 1. BETA BLOCKERS e.g. propranolol 2. TCAs e.g. amitriptyline 3. Anti-convulsant e.g. topiramate
80
Triptan MOA
5-HT receptor at trigeminal nerve, prevents neuropeptide release that would lead to - vasodilation - neurogenic inflammation - PAIN on cranial vasculature, leading to vasoconstriction
81
Cluster headache definition
Episodic headaches lasting from 7 days up to 1 year (usually 2-3 weeks) with pain-free periods that last around 4 weeks Considered the MOST DISABLING of primary headaches
82
Cluster headache epidemiology
Much rarer than migraines More common in MALES (x4) Typically affects adults with onset 20-40 years
83
Cluster headache risk factors
SMOKER ALCOHOL Male Genetics (FHx)
84
Px of cluster headache
RAPID ONSET EXCRUCIATING PAIN, CLASSICALLY AROUND THE EYE - other common areas = temples or forehead UNILATERAL and LOCALISED PAIN - rises to a crescendo IPSILATERAL AUTONOMIC FEATURES - watery & bloodshot eye - miosis +/- ptosis
85
Management of acute cluster headache attack
15L 100% O2 for 15 minutes via non-rebreather mask TRIPTANS e.g. SUMATRIPTAN (Analgesics are UNHELPFUL)
86
Cluster headache prevention
1st LINE: VERAPAMIL (CCB) Prednisolone Reduce alcohol consumption & stop smoking
87
Is a tension headache episodic or chronic?
Usually chronic but can be episodic - episodic <15 days/month - chronic >15 days/month (for atleast 3 months)
88
Tension headache triggers
``` Stress Sleep deprivation Bad posture Hunger Eyestrain Anxiety Noise ```
89
Tension headache Px
Usually at least 1 of the following: - BILATERAL - Pressing/tight & NON-PULSATILE (like an elastic band) - mild/moderate intensity NO AURA, vomiting, or sensitivity to head movement can be "pressure" behind eyes but the pain isn't localised here
90
Tension headache Mx
Avoidance of triggers & stress relief Symptomatic relief: NSAIDs (aspirin, ibuprofen), paracetamol AVOID OPIOIDS limit analgesics to no more than 6 days per month to reduce the risk of medication-overuse headaches
91
Examples of secondary headaches
``` Giant cell/temporal arteritis Sentinel headache Thunderclap headache Trauma Medication overuse Trigeminal neuralgia Systemic infection Meningitis ```
92
Epilepsy diagnostic criteria
At least 2 UNPROVOKED seizures occurring MORE THAN 24 HOURS apart
93
Epilepsy aetiology
2/3rds are IDIOPATHIC ``` Other: Cortical scarring e.g. trauma, stroke, infection Tumours/space-occupying lesions Alzheimer's Alcohol withdrawal (delirium tremens) ```
94
Epilepsy risk factors
FHx Premature birth Abnormal cerebral blood vessels Drugs e.g. cocaine
95
Aura in seizures
Part of the seizure where the patient is AWARE and often PRECEDES other manifestations - e.g. strange feelings in gut, deja vu, strange smells, flashing lights - often implies a PARTIAL SEIZURE
96
Post-ictal period of seizures
PERIOD AFTER SEIZURES Headache, confusion, myalgia, sore tongue (often bitten) Post-ictal Todd's palsy = temporary weakness after focal seizure in MOTOR CORTEX Dysphagia following temporal lobe seizure
97
Types of seizure
Primary generalised (40%) - generalised = whole cortex - ALWAYS ASSOCIATED WITH LOSS OF CONSCIOUSNESS & LACK OF AWARENESS - BILATERAL and SYMMETRICAL motor manifestations Partial (focal) (60%) - SINGLE LOBE IN ONE HEMISPHERE e.g. temporal lobe - often seen with underlying structural disease - may later progress to generalised
98
Types of primary generalised seizure
Tonic = rigid, stiff limbs Clonic = rhythmic muscle jerking TONIC-CLONIC (Grand Mal) = stereotypical shaking seizures Myoclonic = isolated jerking of a limb Atonic = opposite to tonic: loss of muscle tone (floppy) Absence (Petit Mal) = blank stare, common in childhood + increases risk of developing tonic-clonic as adult
99
Types of partial (focal) seziure
Simple partial seizure = no effect on consciousness or memory, no post-ictal symptoms Complex partial seizure = memory/awareness is affected at some point, most commonly TEMPORAL (speech, memory, emotion), post-ictal confusion in temporal (frontal has swift recovery) Partial seizure with secondary generalisation = 2/3 patients with partial seizures will develop generalised (usually T-C)
100
Temporal lobe seizure characteristics
AURA (80%) Automatisms e.g. lip smacking Anxiety, out-of-body experiences
101
Frontal lobe seizure characteristics
Motor features e.g. posturing, peddling legs JACKSONIAN MARCH (seizures march up/down the motor homunculus) Post-ictal Todd's palsy (starts distally in a limb and works its way up to the face)
102
Parietal lobe seizure characteristics
Sensory disturbances e.g. tingling/numbness
103
Occipital lobe seizure characteristics
Visual phenomena e.g. spots, lines, flashes
104
Non-epileptic seizure characteristics
Entirely situational e.g. metabolic disturbances, low Na+, hypoxia Typically longer with closed eyes + mouth DO NOT OCCUR DURING SLEEP do not involve incontinence or tongue biting Pre-ictal anxiety symptoms
105
Epilepsy Ix
ELECTROENCEPHALOGRAM (EEG) Not diagnostic but can help support a diagnosis/type of epilepsy MRI/CT HEAD - rules out other potential causes e.g. space-occ lesion BLOODS - rules out other potential causes e.g. metabolic Genetic testing e.g. juvenile myoclonic epilepsy
106
Wernicke's encephalopathy
Depletion of thiamine (Vitamin B1) Classic triad: Confusion Ataxia Opthalmoplegia Sign: Asterixis (liver flap) - sign of metabolic encephalopathy
107
Epilepsy Tx: generalised tonic-clonic, tonic, atonic
Sodium valproate for males & women unable to bear children Lamotrigine for females of childbearing potential
108
Epilepsy Tx: myoclonic
Sodium valproate for males & women unable to bear children Levetiracetam/Topiramate for females of childbearing potential
109
Epilepsy Tx: absence
Sodium valproate for males & women unable to bear children Ethosuximide for females of childbearing potential
110
Epilepsy Tx: partial (focal)
Lamotrigine
111
Example of primary brain tumour
Much less common than secondary Gliomas e.g. astrocytoma (most common) Others e.g schwannoma
112
Most common origins of secondary brain tumours
``` Non-small cell lung cancers (most common) SCLC Breast Renal cell carcinoma GI ```
113
Alzheimer's disease epidemiology
Most common type of dementia | Mainly affects >65
114
Parkinson’s disease patho
Progressive destruction of dopaminergic neurones in the substantia nigra of the basal ganglia Basal ganglia = habitual movements, voluntary movements + learning of specific movement patterns
115
Clinical Px Parkinson’s disease
TRIAD: Unilateral RESTING tremor (pill-rolling) - diminishes with intentional movement Cogwheel rigidity (resistance to passive movement of the joint) Bradykinesia: shuffling gait + ‘freezing’ when starting to walk (difficulty initiating movement) Cognitive impairment Depression Visual hallucinations Sleep disorders NO WEAKNESS
116
PD Ix
DaT scan (injected drug assesses dopaminergic neurones) A normal CT scan will show no pathology
117
PD Mx
1. Dopamine agonists e.g. carbergoline 2. MAO-B inhibitors e.g. sergeline 3. Co-careldopa (Levodopa + carbidopa)
118
PD vs Benign resting tremor
PD: worse at rest, improves with intentional movement BRT: improves at rest, improves with ALCOHOL, worse with intentional movement
119
Parkinson’s histopathological findings
``` Loss of dopaminergic neurones Lewy bodies (eosinophilic cytoplasmic inclusions made of alpha synuclein) ```
120
Huntingtons disease
HTT mutation on c4 = CAG trinucleotide repeat >35 CAG = HD Loss of GABAergic neurones = hyperexcitation of dopaminergic pathways in the striatum = excessive thalamic stimulation = chorea
121
Clinical Px of HD
``` Chorea Dystonia Incoordination Cognitive + behaviour difficulties Irritability, agitation, anxiety ```
122
HD Ix
GENETIC TESTING MRI/CT = loss of striatal volume
123
HD Tx
Benzodiazepines/valproic acid (for chorea) SSRIs (for depression) Haloperidol (for psychosis)
124
HD prognosis
Poor Most common cause of death = pneumonia Second most common cause of death = suicide
125
Differential diagnosis in HD
Sydenham's chorea (Rheumatic fever)
126
Alzheimer's disease RFs
Down's syndrome Depression ApoE E4 allele homozygosity
127
Pathological hallmarks of AD
EXTRACELLULAR deposition of B-amyloid plaques | INTRACELLULAR neurofibrillary tangles (tauopathy)
128
Alzheimer's treatment
Acetycholinesterase inhibitors e.g. rivastigmine, donepezil
129
AD Ix
Entirely clinical diagnosis MRI = cerebral atrophy Rule out: bloods (TFTs, B12)
130
Vascular dementia
Caused by MULTIPLE INFARCTS Sudden onset Stepwise deterioration
131
Lewy body dementia
Presence of Lewy Bodies in brainstem + occipto-parietal region (misfolded a-synuclein/eosinophilic inclusions) Fluctuating cognitive dysfunction, visual hallucinations + parkinsonism Tx: cholinesterase inhibitors
132
Frontotemporal dementia
``` Progressive More common dementia in those under 65 Atrophy in frontal and temporal lobes with no plaque formation Tauopathy (which leads to apoptosis) Pick bodies ``` Px: behavioural issues e.g. disinhibition, progressive aphasia e.g. slow, difficult speech, dementia symptoms Tx: cholinesterase inhibitors
133
Age of onset multiple sclerosis
Early adult life (20-40 years)
134
Pathophysiology of multiple sclerosis
``` Autoimmune destruction (CD4 mediated - Type 4 HS) CNS oligodendrocyte myelin sheath attack = plaques (sclera) Remission = regulatory T cells > remyelination in early disease ```
135
MS patterns
Relapsing remitting (most common) Primary progressive Secondary progressive Progressive relapsing
136
Charcot’s neurological triad (MS)
Nystagmus (painful, shaking eyes) - optic nerve plaques: optic neuritis Intention tremor - motor pathway plaques Staccato speech (dysarthria) - brain stem attacks: conscious movement (eating, talking) + unconscious (swallowing)
137
What is Uhthoff’s phenomenon in MS?
Worsening symptoms with increase in body temperature
138
What is Lhermitte’s sign in MS?
Sudden electrical sensation passing down the neck, spine, radiating out to the limbs when bending the neck forward
139
McDonald’s diagnostic criteria for MS
2 or more CNS attacks, at least 30 days apart and affecting different parts of the CNS “Disseminated in space and time”
140
MS Ix
Clinical diagnosis LUMBAR PUNCTURE: Oligoclonal IgG bands MRI: plaque detection, white matter abnormalities, periventricular lesions
141
MS Tx
Acute: IV METHYLPREDNISOLONE ``` Other: Vitamin D supplements B-IFN (decreases inflammatory cytokines in brain) Biologicals e.g. Monoclonal antibodies Symptomatic: baclofen, amitriptyline DMARDs ```
142
Px MS
``` TEAM: Tingling (parathaesia) Eye: optic neuritis Ataxia Motor: paraparesis ``` Autonomic: bladder and bowel, sexual dysfunction Decreased vibration sense Dysphagia, constipation Falls
143
Risk factors MS
Genetic: female, HLA DR2 Environmental: infections, vitamin D deficiency
144
UMN symptoms in MND
EVERYTHING GOES UP Increased muscle tone Brisk reflexes Positive BABINSKI sign Impaired fine movement
145
LMN symptoms in MND
EVERYTHING GOES DOWN Decreased muscle tone and reflexes Muscle WASTING Fasciculations
146
MND epidemiology
>50 y/o males
147
Typical MND patient Px
``` >40 Stumbling, spastic gait FOOT DROP, weak grip NO SENSORY LOSS NO EYE MOVEMENT DISTURBANCES ```
148
Types of MS
``` ALS: UMN+LMN PBP (progressive bulbar palsy): UMN+LMN PMA (progressive muscular atrophy): LMN only PLS (primary LS): UMN only Corticobulbar (pseudobulbar) palsy ```
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ALS Px
MOST COMMON Weakness, UMN + LMN signs, fasciculations Drifting thumb Wrist, foot drop
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Progressive bulbar palsy Px
WORST PROGNOSIS Affects cranial nerves IX-XII Dysarthria, dysphagia
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Progressive muscular atrophy Px
Only LMN signs | Affects muscles distally to proximally
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MND Ix
Clinical diagnosis: LMN + UMN signs in 3 regions Blood tests MRI Lumbar puncture
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MND Tx
Antiglutamatergic drugs e.g. RILUZOLE (sodium channel blocker that inhibits glutamate release) Spasticity: baclofen Respiratory: non-invasive ventilation
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What is myasthenia gravis?
Autoimmune destruction of acetylcholine receptors
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What is myasthenia gravis exacerbated by?
Pregnancy Infection Emotion Drugs
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Myasthenia gravis Px
Symptoms worse after muscle use (increasing muscle fatigue)
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Myasthenia gravis Ix
Acetylcholine receptor (ACh-R) antibodies (85% of patients) Positive tensilon test - edrophonium (neostigmine) injection = temporary relief (due to increase in ACh) A CT or MRI of the thymus gland to look for a thymoma
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Myasthenia gravis Tx
Immunosuppression Neostigmine Thymectomy
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Guillane-Barré pathophysiology
Peripheral neuropathy often occurring after infection (molecular mimicry against pathogenic antigen AND peripheral nerves)
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Kernigs sign
Resistance to extension of the leg while the hip is flexed +ve in meningitis
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Brudinskis sign
Flexion of the hips and knees in response to neck flexion +ve in meningitis
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Syncope
Temporary loss of consciousness due to disruption of blood flow to the brain (Vasovagal)
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Primary syncope
Dehydration Missed meals Extended standing in a warm environment Stimuli E.g. sight of blood
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Syncope Ix
ECG 24 hour ECG Echocardiogram Bloods
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Spina bifida aetiology
Combination of genetic, nutritional and environmental risk factors e.g. folate deficiency
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Autonomic vs somatic NS receptors
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Cerebral stroke patterns: MCA vs ACA
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Tonic seizure
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Tonic clonic seizure
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Selective colour vision deficit on red-green colour test
MS
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Most common causative organism of meningitis in children 3 months-12 years
Strep pneumoniae (think snotty kids)
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Saddle anaesthesia
Associated with CAUDA EQUINA SYNDROME Erectile dysfunction Loss of bowel control
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Change in CSF parameters BACTERIAL meningitis
Turbid (yellow) fluid, with neutrophils, raised protein (bacteria produce enzymes etc), low glucose
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Change in CSF parameters VIRAL meningitis
Clear fluid, with lymphocytes, normal glucose, normal protein
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Change in CSF parameters in FUNGAL meningitis
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Change in CSF parameters TB meningitis
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Uhthoff's phenomenon
MS symptoms get worse with heat (E.g. shower)
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Resperidone
Dopamine receptor antagonist: manages aggression and chorea in HD
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Guillain Barre syndrome Tx
IV immunoglobulins
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Encephalitis
Inflammation of the brain Can be caused by herpes simplex virus Triad: fever, altered mental state, headache Community Tx: IM Benpen (suspect meningitis) Hospital: acyclovir
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Shingles (Herpes Zoster) neurological manifestation
Post-herpetic neuralgia
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Sciatica
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Trigeminal neuralgia
Sudden severe facial pain in the trigeminal regions
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Difference between Lambert Eaton syndrome and myasthenia gravis
``` LES = autoimmune attack of calcium gated channels MG = autoimmune attack of ACh receptor ```
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Brown Sequard syndrome
Ipsilateral loss: Corticospinal Dorsal column Contralateral (1-2 levels down): Spinothalamic
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Charcot-Marie-Tooth syndrome
Autosomal dominant Demyelination of peripheral motor and sensory nerves Classical features: inverted champagne bottle legs, high foot arches
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Duchenne Muscular dystrophy
X-linked recessive disease (only men can be affected) Characterised by progressive muscle degeneration and weakness due to the alterations of a protein called dystrophin that helps keep muscle cells intact
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Beckers muscular dystrophy
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Cauda equina vs conus medullaris
Cauda Equina = L1/L2 (level at which spinal cord terminates) = LMN features only Conus medullaris = UMN features (hyperreflexic)
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Stroke definition
Sudden onset neurological deficit due to ischaemic or haemorrhagic compromise with symptoms lasting over 24 hours