Neurology Flashcards
Lesion in brain causes what type of weakness?
Contralateral, one-sided weakness
Lesion in SC causes what type of weakness?
B/L weakness
Signs of UMNL
Hyperreflexia
Hypertonia
Clonus
Hemiplegic gait (circumduction/scissoring)
Signs of LMNL
Hypotonia
Hyporeflexia
Fasciculations
High stepping gait (foot drop)
Features of NMJ disorder
Fatiguable weakness
What is a stroke?
Sudden onset neurological deficit caused by reduced blood supply to the brain
Epidemiology of stroke?
4th most common disorder in UK
20% mortality
40% of people with become dependent for 6 months following
Risk factors for a stroke?
Modifiable: BP, smoking
Non-modifiable: age, sex, ethnicity
Types of stroke?
Ischaemic (80%)
Haemorrhagic (20% - intracerebral, subarachnoid)
How to classify stroke?
Oxford Bamford - TACI, PACI, POCI, Lacunar
What classifies a TACI?
A total anterior circulation stroke (TACS) is a large cortical stroke affecting the areas of the brain supplied by both the middle and anterior cerebral arteries.
All three of the following need to be present for a diagnosis of a TACS:
Unilateral weakness (and/or sensory deficit) of the face, arm and leg Homonymous hemianopia Higher cerebral dysfunction (dysphasia, visuospatial disorder)
What classifies a PACI?
A partial anterior circulation stroke (PACS) is a less severe form of TACS, in which only part of the anterior circulation has been compromised.
Two of the following need to be present for a diagnosis of a PACS:
Unilateral weakness (and/or sensory deficit) of the face, arm and leg Homonymous hemianopia Higher cerebral dysfunction (dysphasia, visuospatial disorder)
What classifies a POCI?
A posterior circulation syndrome (POCS) involves damage to the area of the brain supplied by the posterior circulation (e.g. cerebellum and brainstem).
One of the following need to be present for a diagnosis of a POCS:
Cranial nerve palsy and a contralateral motor/sensory deficit
Bilateral motor/sensory deficit
Conjugate eye movement disorder (e.g. horizontal gaze palsy)
Cerebellar dysfunction (e.g. vertigo, nystagmus, ataxia)
Isolated homonymous hemianopia
What classifies a Lacunar stroke?
A lacunar stroke (LACS) is a subcortical stroke that occurs secondary to small vessel disease. There is no loss of higher cerebral functions (e.g. dysphasia).
One of the following needs to be present for a diagnosis of a LACS:
Pure sensory stroke
Pure motor stroke
Sensori-motor stroke
Ataxic hemiparesis
How to diagnose stroke?
FAST/ROSIER
Non-contrast CT head, if ischaemic then MRI
How to treat stroke?
MDT
Ischaemic - <4.5 hours thrombolysis, <6 hours thrombectomy, 300mg aspirin - 75mg clopidogrel
Haemorrhagic - control BP, stabilise, reverse anti-coag
Other - statin, AF (anticoagulant 2 weeks), Barthel index, driving, lifestyle
Absolute contraindications for thrombolysis?
- Previous intracranial haemorrhage
- Seizure at onset of stroke
- Intracranial neoplasm
- Suspected subarachnoid haemorrhage
- Stroke or traumatic brain injury in preceding 3 months
- Lumbar puncture in preceding 7 days
- Gastrointestinal haemorrhage in preceding 3 weeks
- Active bleeding
- Pregnancy
- Oesophageal varices
- Uncontrolled hypertension >200/120mmHg
Effects of lesion in middle cerebral artery?
Arms
Speech - Aphasia
Contralateral hemiparesis and sensory loss, upper extremity > lower
Contralateral homonymous hemianopia
Effects of lesion in anterior cerebral artery?
Legs
Behaviour
Contralateral hemiparesis and sensory loss, lower extremity > upper
Effects of lesion in posterior cerebral artery?
Vision disturbances (Contralateral homonymous hemianopia with macular sparing, Visual agnosia)
Ataxia
Effects of lesion in basilar artery?
Locked in syndrome
Effects of lesion in lateral medullary artery? (Wallenberg syndrome)
Horners
Ipsilateral pain/temperature loss on face, ataxia, nystagmus, dysphagia
Contralateral pain/temperature loss on body
Effects of Weber stroke?
ipsilateral III palsy
contralateral motor weakness
Effect of lacunar stroke?
present with either isolated hemiparesis, hemisensory loss or hemiparesis with limb ataxia
strong association with hypertension
common sites include the basal ganglia, thalamus and internal capsule
What is a TIA?
Temporary sudden onset neurological deficit, caused by a sudden reduction in blood supply to the brain, causes ischaemia NOT infarction
Types of TIA
Anterior (carotid 80%) = contralateral hemiparesis, monocular blindness, dysphasia
Posterior (vertebrobasilar 20%) = vertigo, dysarthria, diplopia, ataxia
How to manage TIA?
<7 days = aspirin 300mg, don’t drive, see specialist 24 hours
>7 days = aspirin 300mg, don’t drive, see specialist in next 7 days
Differentials of stroke? (BEHIND)
B = brain - SOL E = epilepsy H = hypoglycaemia/ natraemia I = infection (meningitis) N = neuro (MS, hemiplegic migraine) D = disc prolapse
What is multiple sclerosis?
Autoimmune demyelination of the oligodendrocytes in the white matter tracts of the CNS
Who does MS affect?
F>M
20-40’s
Risk factors for MS?
Higher latitude/less sunlight
EBV
Smoking
Types of MS
Relapsing-Remitting
Secondary Progressive
Primary Progressive
How to diagnose MS?
MRI (T2 flair)
Lumbar puncture (oligoclonal bands)
Vision-evoke response
Management of MS?
Acute = methylprednisolone
Prevention = beta-interferon
MDT!
What is MND?
A disorder that affects both UMN & LMN without causing any sensory involvement
Causes of MND?
Unknown, links to mutation SOD-1 gene
Who gets MND?
M>F
Middle aged
Sporting individuals
Symptoms of MND?
C-Spine (split hand)
Thoracic (type 2 resp failure, nocturnal hypoventilation)
Lumbar (foot drop)
Types of MND?
ALS
PMA
PLS
Pseudo/bulbar
Complications of MND?
Respiratory failure
Starvation
Aspiration
Diagnosis of MND?
Clinical
Blood test - SOD-1
EMG
Nerve conduction - normal
Treating MND?
Prognosis - riluzole
Secretions - carbocistine, hyoscine patches, botox
Choking - buccal midazolam
MDT!
What is Parkinson’s?
Neurological disorder, caused by the reduction of the dopaminergic neurones of the pars compact of the substance nigra in the basal ganglia. This leads to rigidity and issues with movement.
Who does Parkinson’s affect?
M>F
Elderly (early onset <55 years)
Risk factors for Parkinson’s?
Smoking
FHx
Diagnosis for Parkinson’s?
Clinical
Lying and standing BP
Vision
DAT scan
Management of Parkinson’s?
MDT!
if the motor symptoms are affecting the patient’s quality of life: levodopa
if the motor symptoms are not affecting the patient’s quality of life: dopamine agonist (non-ergot derived, e.g., ropinirole), levodopa or monoamine oxidase B (MAO‑B) inhibitor
Differentiate between idiopathic and drug-induced Parkinsonism?
Idiopathic Parkinson’s - unilateral Sx
Drug-induced - bilateral Sx
CSF analysis positive for bacteria?
Appearance - cloudy Glucose - low (<1/2 plasma) Protein - high (>1g/l) White cells - 10 - 5,000 polymorphs/mm³ Cultures - positive Cell differential - neutrophil predominance Opening pressure - elevated
CSF analysis positive for virus?
Appearance - clear/cloudy
Glucose - normal
Protein - normal/raised
White cells - 15 - 1,000 lymphocytes/mm³
Cultures - negative
Cell differential - lymphocyte predominance
Opening pressure - normal/slightly elevated
CSF analysis positive for fungus?
Appearance - cloudy Glucose - Low Protein - high White cells - 20 - 200 lymphocytes/mm³ Cultures - positive (fungal) Cell differential - lymphocyte predominance Opening pressure - elevated
CSF analysis positive for tuberculosis?
Appearance - slightly cloudy, fibrin web Glucose - Low Protein - very high White cells - 30 - 300 lymphocytes/mm³ Cultures - positive (AFB) Cell differential - lymphocyte predominance Opening pressure - variable
What is epilepsy?
When you have 2 or more unprovoked seizures
Seizure = hyper excitability of cortical neurones that leads to transient changes in behaviour and EEG findings
Who is at risk of epilepsy?
3-4% background risk of having a seizure
70% only ever have one seizure
Classifying seizures?
Seizure type
Epilepsy type
Epilepsy syndrome
General treatment of epilepsy?
Anti-epileptic
Avoid triggers
Safety - driving, heights, open water swimming
Pregnancy advice
How to differentiate between a true seizure and pseudo seizure?
Prolactin
Elevated serum prolactin 10 to 20 minutes after an episode can be used to differentiate a general tonic-clonic/partial seizure from a non-epileptic pseudo seizure. True epileptic seizure = raised serum prolactin
What drugs can cause idiopathic intracranial hypertension>?
combined oral contraceptive pill steroids tetracyclines vitamin A lithium
Laughter → fall/collapse ?
Cataplexy
Around two-thirds of patients with narcolepsy have cataplexy.
What is tuberous sclerosis?
is a genetic condition of autosomal dominant inheritance. Like neurofibromatosis, the majority of features seen in TS are neurocutaneous.
Cutaneous features
- depigmented ‘ash-leaf’ spots which fluoresce under UV light
- roughened patches of skin over lumbar spine (Shagreen patches)
- adenoma sebaceum (angiofibromas): butterfly distribution over nose
- fibromata beneath nails (subungual fibromata)
- café-au-lait spots* may be seen
Tx of brain abscess
IV 3rd-generation cephalosporin + metronidazole
First line Tx for neuropathic pain
amitriptyline, duloxetine, gabapentin or pregabalin.
If one of these agents don’t work next line is to try one of the other remaining three drugs
What sign is seen on venography for sagittal sinus thrombosis
‘empty delta sign’
CN IV palsy
defective downward gaze (which may present as an upward deviation of the eye) and vertical diplopia (i.e. double vision where the images are on top of or diagonally displaced from each other)
Additionally, patients with a CN IV palsy will often adopt an abnormal head posture, in which the head is tilted away from the side of the lesion. This is to compensate for the weakened medial rotation, which helps to reduce the diplopia they experience.
Neuroimaging findings of normal pressure hydrocephalus
ventriculomegaly in the absence of, or out of proportion to, sulcal enlargement
Lambert Eaton vs Myasthenia Gravis
Weakness in Lambert Eaton improves after exercise, unlike myasthenia gravis; which worsens after exercise.
Features or lambert eaton:
* repeated muscle contractions lead to increased muscle strength (in contrast to myasthenia gravis)
* in reality, this is seen in only 50% of patients and following prolonged muscle use muscle strength will eventually decrease
* limb-girdle weakness (affects lower limbs first)
* hyporeflexia
* autonomic symptoms: dry mouth, impotence, difficulty micturating
* ophthalmoplegia and ptosis not commonly a feature (unlike in myasthenia gravis)
Which extra-ocular muscles are innervated by the contralateral side
SUPERIOR ones - so SUPERIOR oblique (CN IV) and SUPERIOR rectus (CN III).
What CN’s are affected by vestibular schwannomas
Cranial nerves V, VII and VIII
Temporal arteritis vs trigeminal neuralgia
Temporal arteritis vs trigeminal neuralgia: the onset is subacute (2 weeks - blindness happens a lot faster), temporal arteritis causes a headache typically; severe stabbing pain in the trigeminal distribution triggered by shaving is very typical
Trigeminal Neuralgia -not serious -evoke by light touch (classic) -no eye, ear problem -no systemic symptom Temporal arteritis -serious -jaw claudication (classic) -vision problem, tender temporal artery -systemic symptom (eg. Fever, anorexia, night sweats) -extra hint : Polymyalgea rheumatica : proxumal muscle pain
Cushing reflex
a physiological nervous system response to increased intracranial pressure (ICP) that results in hypertension and bradycardia
What Tx for suspected encephalitis
Aciclovir
CN VI palsy
defective eye abduction and horizontal diplopia
Bitemporal hemianopia causes
UP LOC
Upper quadrant Pituitary, LOwer quadrant Craniopharyngioma
PITS mnemonic: Parietal = Inferior, Temporal = Superior
- lesion of optic chiasm
- upper quadrant defect > lower quadrant defect = inferior chiasmal compression, commonly a pituitary tumour
- lower quadrant defect > upper quadrant defect = superior chiasmal compression, commonly a craniopharyngioma
Cause of Saturday night palsy
caused by compression of the radial nerve against the humeral shaft, possibly due to sleeping on a hard chair with his hand draped over the back
Tx of spasticity in MS
Baclofen and gabapentin
Lumbar puncture in GBS
is a useful diagnostic investigation as the finding of elevated protein with normal white cell count is found in up to 90% of patients in the first week of illness, and this finding combined with a classical history is highly suggestive of GBS.
Features of complex regional pain syndrome
- progressive, disproportionate symptoms to the original injury/surgery
- allodynia
- temperature and skin colour changes
- oedema and sweating
- motor dysfunction
- the Budapest Diagnostic Criteria are commonly used in the UK
Gold standard test for cervical myelopathy
MRI of cervical spine
It may reveal disc degeneration and ligament hypertrophy, with accompanying cord signal change
Features of Bell’s palsy
- lower motor neuron facial nerve palsy - forehead affected
- in contrast, an upper motor neuron lesion ‘spares’ the upper face
- patients may also notice post-auricular pain (may precede paralysis), altered taste, dry eyes, hyperacusis
Features of temporal lobe seizure
Lip smacking + post-ictal dysphasia
Broca’s dysphasia
speech non-fluent, comprehension normal, repetition impaired. Is left inferior frontal gyrus
Be (Brocas) Expressive in (inferior) front (frontal) of Everyone
Tx of restless leg syndrome
dopamine agonists such as ropinirole
First-line treatment to children , young people and adults with absence seizures
Ethosuximide
Sodium Valproate
Managing tremor in drug-induced Parkinsonism
Procyclidine
First line treatment for childcare, young people and adults with newly diagnosed focal seizures
Carbamazepine
Lamotrigine
Gold standard investigation for suspected vestibular Schwannomas
audiogram and gadolinium-enhanced MRI head scan
Painful third nerve palsy?
Posterior communicating artery aneurysm
Common cause of brain abscess
ascending infection from middle ear of from facial sinuses.
What is Charcot-Marie-Tooth Disease
most common hereditary sensorimotor neuropathy.
There is a clear description of the inverted champagne bottle sign and pes cavus as well as a family history which points to CMT over chronic inflammatory demyelinating polyneuropathy.
Causes of ataxic gaits
Wide-based gait with loss of heel to toe walking
Occur following cerebellar injury
PASTRIES
P - Posterior fossa tumour A - Alcohol S - Multiple sclerosis T - Trauma R - Rare causes I - Inherited (e.g. Friedreich's ataxia) E - Epilepsy treatments S - Stroke
What is thoracic outlet syndrome
typically presents with muscle wasting of the hands, numbness and tingling and possibly autonomic symptoms
a disorder involving compression of brachial plexus, subclavian artery or vein at the site of the thoracic outlet.
TOS can be neurogenic or vascular; the former accounts for 90% of the cases
What makes MG worse
All ( kind of ) A’s
AED: Phenytoin Abx: Gent, Macro, Quino, Tetra Antiarrhythmic: Quinidine, Procainamide Anti-manic: Lithium Anti-HR: BB Anti-Wilson's Disease: Penicillamine
Features of Wernicke’s dysphasia
speech fluent, comprehension abnormal, repetition impaired
When can you stop AEDs
Can be considered if seizure free for > 2 years, with AEDs being stopped over 2-3 months
Tx of symptomatic chronic subdural bleeds
Burr hole evacuation
How to diagnose (and assess degree of stenosis) of carotid artery stenosis
Duplex ultrasound
What blood tests to do if under 55 presents with no obvious cause of a stroke
thrombophilia and autoimmune screening
Todd’s paresis
Post-ictal weakness after focal seizures
What drug to avoid in myasthenia gravid?
Beta-blockers
Hypsarrhytmia on EEG
infantile spasms (West’s syndrome)
Management of MG
- long-acting acetylcholinesterase inhibitors
- pyridostigmine is first-line
- immunosuppression is usually not started at diagnosis, but the majority of patients eventually require it in addition to long-acting acetylcholinesterase inhibitors:
- prednisolone initially
- azathioprine, cyclosporine, mycophenolate mofetil may also be used
- thymectomy
Causes of reduced reflexes and upping planters
MND, syringomelia, subacute combined degeneration of cord, Friedrich’s ataxia
Features of subarachnoid haemorrhage
SAH commonly presents with a thunderclap headache at the back of the head.
It is more common in the elderly or alcoholics as they have more fragile veins that will rupture more easily.
Plain CT shows a classic ‘starfish’ sign often
Features of cavernous sinus thrombosis
The common presentation for this is sudden onset frontal headache.
Commonly cavernous sinus thrombosis arises due to the retrograde spread of infection from the face, and this may be identifiable in the history.
Features of subdural haemorrhage
This is commonly caused by trauma, but can sometimes arise as a result of an aneurysm rupture. In these cases, it will present with a thunderclap headache.
There may also be signs of mass effect such as cognitive dysfunction, visual disturbances of respiratory depression.
This will be visible on plain CT as a crescentic hyperattenuated lesion that crosses suture lines.
What is neuroleptic malignant syndrome
It occurs within hours to days of starting an antipsychotic (antipsychotics are also known as neuroleptics, hence the name) and the typical features are:
- pyrexia
- muscle rigidity
- autonomic lability: typical features include hypertension, tachycardia and tachypnoea
- agitated delirium with confusion
