Neurology Flashcards
Pathological basis of meningitis
Inflammation of the pia and arachnoid mater
Microorganisms infect the CSF
Not always an infective cause e.g. can be post surgical
Symptoms of meningitis
TRIAD: Stiffness of the neck, Severe headache, and Fever (infective)
Photophobia
Meningococcal meningitis: petechial non blanching rash
Two most common bacterial causes of meningitis in adults
Diplococcus bacteria: Neisseria Meningitidis (meningococcal meningitis) -ve (non-blanching rash) Streptococcus Pneumoniae (pneumococcal meningitis) +ve
Viral causes of meningitis
Mumps virus
Coxsackie virus
HSV
Drug induced meningitis
NSAIDs
Trimethoprim
Diagnosis of meningitis
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
Treatment for bacterial meningitis
If suspected, give broad spectrum antibiotics before tests come back
Cephalosporins: IV ceftriaxone/IV cefotaxime
Over 50/immunocompromised: add IV amoxicillin
Treatment for viral meningitis
Supportive treatment
Self-limiting in 4-10 days
Acyclovir for HSV meningitis
Types of STROKE
Cerebral infarction (ischaemic stroke)
Intracerebral haemorrhage
Subarachnoid haemorrhage
Transient ischaemic attack Px
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)
TIA epidemiology
MALES
African-Caribbean heritage (HTN and atherosclerosis)
TIA and ischaemic stroke RFs
Age HTN Smoking Diabetes Combined pill Atrial fibrillation Male
Causes of a TIA
Atherothromboembolism
- carotid artery = main cause (carotid bruit)
Cardioembolism
- atrial fibrillation
- post-MI
- valve disease/prosthetic
Hyperviscosity
Hypoperfusion
DDx TIA
Hypoglycaemia Migraine aura Focal epilepsy Vasculitis Syncope
Clinical presentation of a TIA (carotid territory Sx - 90%)
Amaurosis fugax Aphasia Hemiparesis Hemisensory loss Hemianopic visual loss
Amaurosis fugax
Temporary occlusion of retinal artery (temporary retinal hypoxia)
Unilateral sudden vision loss
Transient (minutes)
“like a curtain descending”
ABCD2 score
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
Ix for TIA
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
IMMEDIATE Mx for TIA
Aspirin 300mg
Refer to specialist (within 24h of symptom onset)
Long term Mx of TIA
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%)
Stroke
rapid onset neurological deficit lasting for over 24 hours
poor blood flow to the brain causes cell death
Two types of stroke
Ischaemic (85%)
Haemorrhagic (15%)
1st line Ix: CT HEAD
Penumbra
Infarcted area in ischaemic stroke is surrounded by a swollen area (oedema) which can regain function with neurological recovery
Causes of ischaemic stroke
Small vessel occlusion by thrombus
Atherothromboembolism (e.g. from carotid artery)
Cardioembolism (AF, post-MI, valve disease, IE)
Hyperviscosity
Vasculitis
Hypoperfusion
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
Human homunculus blood supply
ACA (medial supply): lower limbs
MCA (lateral supply): face, upper limbs
Clinical Px of ischaemic stroke (brainstem infarct)
Quadriplegia Locked-in syndrome Facial numbness and paralysis Vision disturbances Vertigo, nausea Cerebellar signs
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)
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
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
Long term ischaemic stroke Mx
Aspirin 300mg for 2 weeks
Clopidogrel daily long term
Anticoagulation (e.g. warfarin) for patients with AF
Rehabilitation
Intracerebral haemorrhage epidemiology
around 10% of strokes
higher mortality: up to 50%
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)
Intracerebral haemorrhage RFs
HYPERTENSION
Anticoagulation
Thrombolysis
Age, Alcohol, Smoking, Diabetes
Two causes of intracerebral haemorrhage
HYPERTENSION: stiff and brittle vessels are prone to rupture + microaneurysms
SECONDARY to ischaemic stroke (bleeding after reperfusion)
Clinical presentation of intracerebral haemorrhage
- similar to ischaemic stroke -
Pointers to haemorrhage: SUDDEN LOSS of consciousness SEVERE HEADACHE MENINGISM COMA
Intracerebral haemorrhage Tx
Stop anticoagulants immediately
Control BP
Reduce ICP
- mechanical ventilation
- IV MANNITOL
Neurosurgical evaluation if:
- hydrocephalus
- coma
- brainstem compression
Vessels in subarachnoid space
circle of willis arteries
Vessels in subdural space
bridging veins (drain from cortex into dural venous sinus > IJV)
Vessels in extradural space
middle meningeal artery
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)
SAH typical age
35-65
RFs associated with berry aneurysms
Polycystic kidney disease
Coarctation of aorta
Connective tissue disorders
SAH RFs
Hypertension Known aneurysm Previous aneurysmal SAH Berry aneurysm RF e.g. PKD Smoking, alcohol
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%)
Complications of SAH
Rebleeding
Hyponatraemia
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
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
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
DDx in SAH
Headache
- MIGRAINE
- Cluster headache
MENINGITIS
Intracerebral haemorrhage
CT scan in SAH
ASAP
Detects >95% of SAH in first 24 hours
Findings of subarachnoid or intraventricular blood
“Star” shaped sign
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)
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
Main cause of subdural haematoma
Head trauma
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)
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
Ix SDH
CT:
- CRESCENT SHAPED (BANANA)
- Unilateral
- MIDLINE SHIFT
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
Ix SDH
CT: Haematoma: - CRESCENT SHAPED (BANANA) - Unilateral - MIDLINE SHIFT
MRI scan
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)
EDH epidemiology
mostly in YOUNG PEOPLE
more common in MALES
EDH pathophysiology
After LUCID INTERVAL:
- rapid rise in ICP
- midline shift
- tentorial herniation
- coning
EDH clinical Px
Lucid interval Rapidly declining GCS (consciousness level) Increasingly severe headache Vomiting Seizures
EDH Ix
CT:
- LENS SHAPED (LEMON)
- Doesn’t cross suture lines (trapped in skull)
- Unilateral
- Midline shift
Skull X-Ray: fractures
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)
EDH Ix
CT: Haematoma: - LENS SHAPED (LEMON) - DOESN'T cross suture lines (trapped in skull) - Unilateral - Midline shift
Skull X-Ray: fractures
What is a migraine?
RECURRENT throbbing UNILATERAL headache often preceded by an AURA and associated NAUSEA, VOMITING, and VISUAL CHANGES
Most common cause of episodic headaches
Migraines
Migraines epidemiology
90% onset before 40 years
More common in females (roughly 3x)
Migraines RFs
Genetics (FHx)
Female
Age (majority of first ones occur in adolescence)
Migraine triggers
CHOCOLATE Chocolate Hangovers Orgasms Cheese Oral contraceptives Lie-ins Alcohol Tumult i.e. loud noises Exercise
Migraine prodrome
yawning, cravings, mood/sleep changes
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
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
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
Migraine Ix
Clinical diagnosis with few or no Ix required
Certain cases may require rule outs e.g. blood tests, CT/MRI, lumbar puncture
Migraine red flag indications for CT/MRI
Thunderclap headache Change in pattern Abnormal neuro exam Onset > 50 years Epilepsy Posteriorly located headache
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
Migraine PROPHYLAXIS
Required if >2 attacks per month OR if acute meds are required >2 per week
Triad:
- BETA BLOCKERS e.g. propranolol
- TCAs e.g. amitriptyline
- Anti-convulsant e.g. topiramate
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
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
Cluster headache epidemiology
Much rarer than migraines
More common in MALES (x4)
Typically affects adults with onset 20-40 years
Cluster headache risk factors
SMOKER
ALCOHOL
Male
Genetics (FHx)
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
Management of acute cluster headache attack
15L 100% O2 for 15 minutes via non-rebreather mask
TRIPTANS e.g. SUMATRIPTAN
(Analgesics are UNHELPFUL)
Cluster headache prevention
1st LINE: VERAPAMIL (CCB)
Prednisolone
Reduce alcohol consumption & stop smoking
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)
Tension headache triggers
Stress Sleep deprivation Bad posture Hunger Eyestrain Anxiety Noise
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
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
Examples of secondary headaches
Giant cell/temporal arteritis Sentinel headache Thunderclap headache Trauma Medication overuse Trigeminal neuralgia Systemic infection Meningitis
Epilepsy diagnostic criteria
At least 2 UNPROVOKED seizures occurring MORE THAN 24 HOURS apart
Epilepsy aetiology
2/3rds are IDIOPATHIC
Other: Cortical scarring e.g. trauma, stroke, infection Tumours/space-occupying lesions Alzheimer's Alcohol withdrawal (delirium tremens)
Epilepsy risk factors
FHx
Premature birth
Abnormal cerebral blood vessels
Drugs e.g. cocaine
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
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
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
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
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)
Temporal lobe seizure characteristics
AURA (80%)
Automatisms e.g. lip smacking
Anxiety, out-of-body experiences
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)
Parietal lobe seizure characteristics
Sensory disturbances e.g. tingling/numbness
Occipital lobe seizure characteristics
Visual phenomena e.g. spots, lines, flashes
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
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
Wernicke’s encephalopathy
Depletion of thiamine (Vitamin B1)
Classic triad:
Confusion
Ataxia
Opthalmoplegia
Sign: Asterixis (liver flap) - sign of metabolic encephalopathy
Epilepsy Tx: generalised tonic-clonic, tonic, atonic
Sodium valproate for males & women unable to bear children
Lamotrigine for females of childbearing potential
Epilepsy Tx: myoclonic
Sodium valproate for males & women unable to bear children
Levetiracetam/Topiramate for females of childbearing potential
Epilepsy Tx: absence
Sodium valproate for males & women unable to bear children
Ethosuximide for females of childbearing potential
Epilepsy Tx: partial (focal)
Lamotrigine
Example of primary brain tumour
Much less common than secondary
Gliomas e.g. astrocytoma (most common)
Others e.g schwannoma
Most common origins of secondary brain tumours
Non-small cell lung cancers (most common) SCLC Breast Renal cell carcinoma GI
Alzheimer’s disease epidemiology
Most common type of dementia
Mainly affects >65
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
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
PD Ix
DaT scan (injected drug assesses dopaminergic neurones)
A normal CT scan will show no pathology
PD Mx
- Dopamine agonists e.g. carbergoline
- MAO-B inhibitors e.g. sergeline
- Co-careldopa (Levodopa + carbidopa)
PD vs Benign resting tremor
PD: worse at rest, improves with intentional movement
BRT: improves at rest, improves with ALCOHOL, worse with intentional movement
Parkinson’s histopathological findings
Loss of dopaminergic neurones Lewy bodies (eosinophilic cytoplasmic inclusions made of alpha synuclein)
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
Clinical Px of HD
Chorea Dystonia Incoordination Cognitive + behaviour difficulties Irritability, agitation, anxiety
HD Ix
GENETIC TESTING
MRI/CT = loss of striatal volume
HD Tx
Benzodiazepines/valproic acid (for chorea)
SSRIs (for depression)
Haloperidol (for psychosis)
HD prognosis
Poor
Most common cause of death = pneumonia
Second most common cause of death = suicide
Differential diagnosis in HD
Sydenham’s chorea (Rheumatic fever)
Alzheimer’s disease RFs
Down’s syndrome
Depression
ApoE E4 allele homozygosity
Pathological hallmarks of AD
EXTRACELLULAR deposition of B-amyloid plaques
INTRACELLULAR neurofibrillary tangles (tauopathy)
Alzheimer’s treatment
Acetycholinesterase inhibitors e.g. rivastigmine, donepezil
AD Ix
Entirely clinical diagnosis
MRI = cerebral atrophy
Rule out: bloods (TFTs, B12)
Vascular dementia
Caused by MULTIPLE INFARCTS
Sudden onset
Stepwise deterioration
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
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
Age of onset multiple sclerosis
Early adult life (20-40 years)
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
MS patterns
Relapsing remitting (most common)
Primary progressive
Secondary progressive
Progressive relapsing
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)
What is Uhthoff’s phenomenon in MS?
Worsening symptoms with increase in body temperature
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
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”
MS Ix
Clinical diagnosis
LUMBAR PUNCTURE: Oligoclonal IgG bands
MRI: plaque detection, white matter abnormalities, periventricular lesions
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
Px MS
TEAM: Tingling (parathaesia) Eye: optic neuritis Ataxia Motor: paraparesis
Autonomic: bladder and bowel, sexual dysfunction
Decreased vibration sense
Dysphagia, constipation
Falls
Risk factors MS
Genetic: female, HLA DR2
Environmental: infections, vitamin D deficiency
UMN symptoms in MND
EVERYTHING GOES UP
Increased muscle tone
Brisk reflexes
Positive BABINSKI sign
Impaired fine movement
LMN symptoms in MND
EVERYTHING GOES DOWN
Decreased muscle tone and reflexes
Muscle WASTING
Fasciculations
MND epidemiology
> 50 y/o males
Typical MND patient Px
>40 Stumbling, spastic gait FOOT DROP, weak grip NO SENSORY LOSS NO EYE MOVEMENT DISTURBANCES
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
ALS Px
MOST COMMON
Weakness, UMN + LMN signs, fasciculations
Drifting thumb
Wrist, foot drop
Progressive bulbar palsy Px
WORST PROGNOSIS
Affects cranial nerves IX-XII
Dysarthria, dysphagia
Progressive muscular atrophy Px
Only LMN signs
Affects muscles distally to proximally
MND Ix
Clinical diagnosis: LMN + UMN signs in 3 regions
Blood tests
MRI
Lumbar puncture
MND Tx
Antiglutamatergic drugs e.g. RILUZOLE (sodium channel blocker that inhibits glutamate release)
Spasticity: baclofen
Respiratory: non-invasive ventilation
What is myasthenia gravis?
Autoimmune destruction of acetylcholine receptors
What is myasthenia gravis exacerbated by?
Pregnancy
Infection
Emotion
Drugs
Myasthenia gravis Px
Symptoms worse after muscle use (increasing muscle fatigue)
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
Myasthenia gravis Tx
Immunosuppression
Neostigmine
Thymectomy
Guillane-Barré pathophysiology
Peripheral neuropathy often occurring after infection (molecular mimicry against pathogenic antigen AND peripheral nerves)
Kernigs sign
Resistance to extension of the leg while the hip is flexed
+ve in meningitis
Brudinskis sign
Flexion of the hips and knees in response to neck flexion
+ve in meningitis
Syncope
Temporary loss of consciousness due to disruption of blood flow to the brain (Vasovagal)
Primary syncope
Dehydration
Missed meals
Extended standing in a warm environment
Stimuli E.g. sight of blood
Syncope Ix
ECG
24 hour ECG
Echocardiogram
Bloods
Spina bifida aetiology
Combination of genetic, nutritional and environmental risk factors e.g. folate deficiency
Autonomic vs somatic NS receptors
Cerebral stroke patterns: MCA vs ACA
Tonic seizure
Tonic clonic seizure
Selective colour vision deficit on red-green colour test
MS
Most common causative organism of meningitis in children 3 months-12 years
Strep pneumoniae (think snotty kids)
Saddle anaesthesia
Associated with CAUDA EQUINA SYNDROME
Erectile dysfunction
Loss of bowel control
Change in CSF parameters BACTERIAL meningitis
Turbid (yellow) fluid, with neutrophils, raised protein (bacteria produce enzymes etc), low glucose
Change in CSF parameters VIRAL meningitis
Clear fluid, with lymphocytes, normal glucose, normal protein
Change in CSF parameters in FUNGAL meningitis
Change in CSF parameters TB meningitis
Uhthoff’s phenomenon
MS symptoms get worse with heat (E.g. shower)
Resperidone
Dopamine receptor antagonist: manages aggression and chorea in HD
Guillain Barre syndrome Tx
IV immunoglobulins
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
Shingles (Herpes Zoster) neurological manifestation
Post-herpetic neuralgia
Sciatica
Trigeminal neuralgia
Sudden severe facial pain in the trigeminal regions
Difference between Lambert Eaton syndrome and myasthenia gravis
LES = autoimmune attack of calcium gated channels MG = autoimmune attack of ACh receptor
Brown Sequard syndrome
Ipsilateral loss:
Corticospinal
Dorsal column
Contralateral (1-2 levels down):
Spinothalamic
Charcot-Marie-Tooth syndrome
Autosomal dominant
Demyelination of peripheral motor and sensory nerves
Classical features: inverted champagne bottle legs, high foot arches
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
Beckers muscular dystrophy
Cauda equina vs conus medullaris
Cauda Equina = L1/L2 (level at which spinal cord terminates) = LMN features only
Conus medullaris = UMN features (hyperreflexic)
Stroke definition
Sudden onset neurological deficit due to ischaemic or haemorrhagic compromise with symptoms lasting over 24 hours
