Neurology Flashcards
What is morton’s neuroma?
A benign neuroma affecting the intermetatarsal plantar nerve, most commonly the third inter-metatarsophalangeal space
Features of morton’s neuroma?
Forefoot pain, worse on walking (like a pebble in their shoe) or a burning paiin
Mulder’s click - hold the neuroma between finger and thumb. Other hand squeezes the metatarsals together. Click may be heard
Distal loss of sensation
How to treat morton’s neuroma?
Avoid high-heels
Metatarsal pad
Corticosteroid injection
Proportion of ischaemic to haemorrhagic stroke
85% ischaemic
15% haemorrhagic
Risk factors of ischaemic stroke
Age HTN Smoking Hyperlipidaemia DM AF
Risk factors for haemorrhagic stroke
Age
HTN
AVM
Anticoagulation therapy
What classification system do we use for strokes?
Oxford Stroke Classification
Bamford classification
Total anterior circulation stroke
A large stroke affecting areas supplied by middle and anterior arteries
Needs all 3 of:
Unilateral weakness (and/or sensory deficit) of face, arm and leg
Homonymous hemianopia
Higher cerebral dysfunction (dysphasia, visuospatial disorder)
Partial anterior circulation stroke
Just the anterior circulation is compromised
2/3 of:
Unilateral weakness (sensory deficit) of face, arm, leg
Homonymous hemianopia
Higher cerebral dysfunction (visuospatial disorder, dysphagia)
Posterior circulation syndrome
Damage to the area of the brain supplied by the posterior circulation
One of the following required:
Cranial nerve palsy + contralateral deficit
Bilateral motor/sensory deficit
Horizontal gaze palsy
Cerebellar dysfunction (vertigo, nystagmus, ataxia)
Isolated homonymous hemianopia
Lacunar syndrome
Subcorticol stroke secondary to small vessel disease
No loss of higher cerebral functions
One of the following: Pure sensory stroke Pure motor stroke Sensori-motor stroke Ataxic hemiparesis
What is the ROSIER score?
A scoring system for stroke. If score is >0, stroke is the likely diagnosis
Aspirin and stroke
Aspirin 300mg orally/rectally as soon as haemorrhagic stroke has been excluded
Thrombolysis
Thrombolysis with alteplase should be given if:
Within 4.5 hours of onset of stroke symptoms
Haemorrhage definitely excluded
Thrombolysis contraindications
Previous intracranial haemorrhage Seizure with stroke Stroke/traumatic brain injury past 3 months Active bleeding GI bleeding type problems
Thrombectomy
Within 6 hours of symptom onset
If ischaemic stroke in the proximal anterior circulation confirmed by CTA/MRA
Statins and anticoagulants
Statins shouldn’t be started till 48 hours after stroke
Anticoagulants shouldn’t be started for 2 weeks after stroke
Secondary prevention of stroke
Clopidogrel 75mg daily
Aspirin plus dipyramidole if clopidogrel is contraindicated
Transient ischaemic attack
A transient episode of neurologic dysfunction caused by focal brain, spinal cord, or retinal ischaemic, without acute infarction
Treatment of TIA
Give aspirin, 300mg immediately
If patient has had multiple TIAs, discuss the need for admission or observation with stroke specialist
Clopidogrel long term
When should carotid artery endarterectomy be considered
Stroke/TIA in carotid territory
Carotid stenosis >70%
What is the first-line investigation in stroke
Non-contrast CT head scan
Extradural haematoma
Collection of blood between the skull and the dura
Extradural haematoma CT scan
Biconvex collection around the edge of the brain (oval coming from the edge)
Features of extradural haematoma
Low impact trauma
LOC
Lucid interval
Rapid decline of consciousness
Dilated pupil due to 3rd cranial nerve compression as a result of mass effects (it also causes uncal herniation)
Treatment of extradural haematoma
Craniotomy
Subdural haematoma
Collection of blood under the dura mater most often caused by trauma (high impact)
CT imaging of subdural haematoma
Crescenteric collection (i.e. following line of the skull)
Treatment for subdural haematoma
Decompressive craniectomy
Burr hole drainage if chronic
Chronic subdural haematoma
Typically presents weeks after mild injury. Patients are often on anticoagulants, or are alcoholics
Patients will have progressive confusion, LOC, weakness etc.
Subarachnoid haemorrhage
A bleed deep to the subarachnoid layer of the meninges
Causes of subarachnoid haemorrhage
Most commonly caused by trauma
If non-traumatic: ruptured aneurysm or AVMs
Features of subarachnoid haemorrhage
Sudden onset severe headache
Neck stiffness
Photophobia
Hydrocephalus
Excessive volume of CSF fluid within the ventricular system of the brain, caused by an inbalance between CSF production and absorption
Symptoms of hydrocephalus
Due to raised ICP:
Headache - worse in the morning (due to lying down)
Nausea/vomiting
Papilloedema
Coma
Obstructive (non-communicating) hydrocephalus
A structural pathology blocks the flow of CSF, causes include:
Tumours
Acute haemorrhage
Developmental abnormalities
Non-obstructive (communicating) hydrocephalus
Due to an imbalance of CSF production and absorption
Increased production:
Choroid plexus tumour (very rare)
Failure of reabsorption at the arachnoid granulations:
Meningitis, post-haemorrhagic
What is normal pressure hydrocephalus
Non-obstructive hydrocephalus with large ventricles but normal ICP
Triad of features in normal pressure hydrocephalus
Dementia
Incontinence
Disturbed gait
Investigating hydrocephalus
CT head first line
MRI head
LP - both diagnostic and therapeutic
When should you not perform LP in hydrocephalus
Obstructive hydrocephalus - difference in pressures between brain and spinal cord will cause brain herniation
Treatment of hydrocephalus
External ventricular drain Ventriculoperitoneal shunt (this treats it long term)
If obstructive, may need surgery
Multiple sclerosis
A chronic cell mediated autoimmune disorder characterised by demyelination in the CNS
MS epidemiology
M:F 1:3
Age 20-40
30% likelihood of twin concordance in monozygotic twins
Relapsing-remitting MS
Most common form
Acute attacks last for 1-2 months, followed by periods of remission
Don’t quite get back to previous function after relapses
Secondary progressive MS
This is where you are relapsing remitting but develop more signs in between relapses
65% of people with relapsing remitting go on to develop secondary progressive
Primary progressive MS
10% of patients
Progressive deterioration from onset
Features of multiple sclerosis
Non-specific features
75% have significant lethargy
Visual:
Optic neuritis
Optic atrophy
Uhthoff’s phenomenon
Sensory
Pins/needles
Numbness
Trigeminal neuralgia
Motor
Spastic weakness
Cerebellar
Ataxia
Other
Urinary incontinence
Sexual dysfunction
Intellectual deterioration
How do we diagnose MS
Lesions disseminated in time and space
Usually an MRI head
Management of MS
Acute relapse:
High dose steroids given for 5 days (methylprednisolone)
Chronic:
DMARDs - beta interferon
Trigeminal neuralgia
Severe unilateral pain
Can be evoked by light touch though also occurs spontaneously
Usually limited to 1 or more sections of the trigeminal nerve
Management of trigeminal neuralgia
Carbamazepine
Referral to neurology if failure to respond
Myasthenia gravis
Autoimmune disorder resulting in insufficienct functioning acetylcholine receptors
Features of myasthenia gravis
Muscle fatigue (that gets worse as the day goes on, is better after rest)
Extraocular muscle weakness - diplopia
Proximal muscle weakness
Ptosis
Dysphagia
Associations with myasthenia gravis
Thymomas Pernicious anaemia RA SLE Thymic hyperplasia in 50-70%
How do we investigate myasthenia gravis
Single fibre electromyography
CT thorax (to exclude thymoma)
Creatine Kinase is NORMAL
Autoantibodies are present in 85-90%
Management of myasthenia gravis
Long-acting anticholinesterase inhibitors - pyridostigmine
Immunosuppression: prednisolone
Thymectomy
Treatment of myasthenic crisis
Plasmapheresis
IV Immunoglobulins
What is Guillain-Barre
An immune mediated demyelination of the peripheral nervous system
Which antibody is associated with Guillain-Barre
Anti-GM1
Features of Guillain-Barre
Progressive weakness of all four limbs
Usually affects lower limbs first
Often triggered by an infection (classically campylobacter jejuni) - so a history of gastroenteritis
Investigations in Gullain-Barre
LP - raised protein with normal WCC
Nerve conduction studies
Can see papilloedema on fundoscopy
What is Miller Fisher syndrome
A variant of Guillain-Barre associated with areflexia, ataxia and ophthalmoplegia
Treatment of Guillain-Barre
IV immunoglobulins
Plasmapheresis
Painkillers
Most people make a full recovery in less than a month
Features of discitis
Back pain Pyrexia Rigors Sepsis Changing lower limb neurology
Causes of discitis
Staphylococcus aureus is most common
Viral
TB
How to diagnose discitis
MRI
Treatment of discitis
IV abx for 6-8 weeks
Complications of discitis
Sepsis
Epidural abscess
What else should we look for in discitis?
Look for bacterial endocarditis
Discitis is usually the result of a bacteraemia
Huntington’s chorea
An autosomal dominant inherited neurodegenerative condition
What is the genetic defect in Huntington’s chorea
Trinucleotide repeat disorder - repeat expansion of CAG
Disease often is seen earlier with each generation due to more repeats
Defect is in Huntingtin gene on chromosome 4
Pathophysiology of Huntington’s chorea
Degeneration of cholinergic and GABAergic neurons in the striatum of the basal ganglia
Features of Huntington’s
Chorea Personality changes Intellectual impairment Dystonia Saccadic eye movements (rapid)
What is chorea
Quick abnormal involuntary movements of hands and feet, comparable to dancing
What is dystonia
Sustained/repetitive muscle contractions resulting in twisting movements and abnormal postures
What can we give for dystonia
Procyclidine, benzos, dopaminergic drugs
What is motor neuron disease
A neurological condition of unknown cause which can present with both upper and lower motor neuron signs
Features of motor neuron disease
No sensory signs
Mixture of upper and lower motor neuron signs
Fasciculations
Unusual to develop <40 years of age
Diagnosis of motor neuron disease
Clinical
Can perform nerve conduction studies to exclude a neuropathy
Amylotrophic lateral sclerosis
50% of motor neuron disease patients
Typically LMN signs in arms
Typically UMN signs in legs
Familial cases - gene responsible is on chromosome 21
Primary lateral sclerosis
Type of motor neuron disease
UMN signs only
Progressive muscular atrophy
Type of motor neuron disease
LMN signs only
Distal before proximal
Best prognosis
Progressive bulbar palsy
Type of motor neuron disease
Palsy of the tongue
Muscles of chewing/swallowing/facial muscle lose function
Carries worst prognosis
Management of motor neuron disease
Riluzole (mainly for ALS) Respiratory care (BIPAP)
Prognosis: poor - 50% of patients die within 3 years
Focal seizures
Start in a specific area on one side of the brain
Focal seizures types
Focal aware (previously called simple partial) Focal impaired awareness (previously called complex partial)
Can be motor (Jacksonian march)
Non-motor (deja vu, jamais vu)
Generalised seizures
Engage or involve both sides of the brain at onset
Generalised seizures types
Motor - generalised tonic-clonic
Non-motor - absence seizures
General rule for prescribing anti-epileptics in epilepsy
Don’t prescribe till 2 seizures
Sodium valproate for generalised
Carbamazepine for partial
Management considerations in epilepsy
Driving - can’t drive for 6 months following seizure (or 12 months if established epileptic)
Pregnancy - anti-epileptics tend to be teratogenic (esp. sodium valproate)
Contraceptives - some anti-epileptics can affect the efficacy of these
When would you start anti-epileptics after a first seizure
If there is a neurological deficit
Brain imaging shows a structural abnormality
EEG shows epileptical activity
Status epilepticus
IV lorazepam
Buccal Midazolam
Rectal diazepam
Give after 5 minutes, then 15 minutes then at 25 minutes give phenytoin or sodium valproate or levitaretam
If after 30 mins still uncontrolled, general anaesthesia
Alcohol withdrawal seizures
Peak incidence 36 hours following cessation of drinking
Related to the GABA mediated inhibition in CNS
Give benzos following cessation of drinking to reduce risk
Psychogenic (pseudoseizures)
Seizure like symptoms but with no electrical discharges
Patients often have a history of mental health problems
Dystrinopathies
X-linked recessive conditions Includes: Becker's Myotonic Duchenne's
Myotonic dystrophy
An inherited myopathy with features developing at around 20-30 years old
Genetics of myotonic dystrophy
Autosomal dominant condition with a trinucleotide repeat disorder:
DM1 - CTG repeat chromosome 19
DM2 - ZNF9 gene repeat on chromosome 3
Difference between myotonic dystrophy DM1 and DM2
Distal weakness more prominent in DM1
Proximal weakness more prominent in DM2
Features of myotonic dystrophy
Frontal balding Myotonic facies (long, haggard) Bilateral ptosis Cataracts Dysarthria
Myotonia Weakness of arms/legs Mild mental impairment DM Testicular atrophy Dysphagia
What is dysarthria
Slow, slurred speech
Parkinson’s
Progressive neurodegenerative condition caused by degeneration of dopaminergic neurons in the substantia nigra
Triad of Parkinson’s symptoms
Bradykinesia
Tremor
Rigidity
(Often asymmetrical)
Bradykinesia in Parkinson’s
Poverty of movement
Short, shuffling steps with reduced arm swing
Difficulty initiating movement
Tremor in Parkinson’s
Resting tremor
Worse when tired/stressed, improves with voluntary movemenet
Typically ‘pill-rolling’ (i.e. thumb and index finger)
Rigidity in Parkinson’s
Lead pipe
Cogwheel - due to superimposed tremor
Extra features of Parkinson’s
Mask-like face Flexed posture Micrographia Drooling of soliva Depression (40%) Dementia, psychoses, sleep disturbance
What drugs typically cause drug induced parkinsonism
Typical antipsychotics
Antiepileptics
Calcium channel blockers
GI prokinetics (domperidone, metoclopromaide)
Treating Parkinson’s disease
Levodopa
Monoamine oxidase B (MAO-B) inhibitor - e.g. selegiline (inhibits breakdown of dopamine)
Why do you not stop levodopa suddenly?
Acute dystonia
Symptoms of lumbar spinal stenosis
Back pain
Neuropathic pain
Claudication like symptoms
Positional pain (e.g. walking up hill better than downhill)
Lumbar spinal stenosis causes
Most commonly degenerative
Tumours
Disk prolapse
Imaging in lumbar spinal stenosis
MRI scanning
Treatment of lumbar spinal stenosis
Laminectomy (removing one or more vertebrae)
Brown-sequard syndrome
Hemisection of spinal cord affecting:
Lateral corticospinal tract
Dorsal columns
Lateral spinothalamic tract
What does the corticospinal tract do?
This is the tract for the motor pathway (upper motor neurons up until they connect with lower motor neurons)
What does the spinothalamic tract do
Sensory:
Gross sensation
Pain
Temperature
What does the dorsal column do
Sensory:
Fine touch
Vibration
Proprioception
Where does the dorsal column decussate
Brainstem
Where does the spinothalamic tract decussate
Level at which they enter the spinal cord
Where does the corticospinal tract decussate
Medulla
Brown sequard syndrome features
Ipsilateral motor loss (spastic paresis)
Ipsilateral vibration and fine touch loss
Contralateral loss of pain and temperature sensation
Spinal cord compression
An oncological emergency that affects up to 5% of patients, usually due to vertebral body metastases
Features of spinal cord compression
Back pain (worse on lying down/coughing) Lower limb weakness Sensory changes Lesions above L1 = UMN signs in legs Lesions below L1 = LMN signs in legs
Treatment of neoplastic spinal cord compression
Dexamethasone
Urgent oncological assessment for need of radiotherapy or surgery
How do we investigate spinal cord compression
MRI whole spine
What is syringomyelia
A collection of CSF within the spinal cord
What causes syringomyelia
A chiari malformation
Trauma
Tumours
Idiopathic
Features of syringomyelia
Cape-like (neck and arms) loss of sensation to temperature but preservation of light touch, proprioception and vibration
(AKA spinothalamic tract affected, NOT dorsal column)
Investigations in syringomyelia
MRI full spine Brain MRI (to rule out Chiari malformation)
What is a Chiari malformation?
A condition in which the brain tissue extends into the spinal canal
It is often associated with syringomyelia (CSF collection in spinal cord)
Treatment of syringomyelia
Shunt
What is acute spinal cord compression characterised by?
Upper motor neurone signs
What is transverse myelitis
Inflammation of both sides of one section of the spinal cord
Causes of transverse myelitis
Infection
Immune system disorders (SLE, Sjrogen’s)
MS
Features of transverse myelitis
Pain - sharp in lower back, may go down legs/arms/abdomen depending on where is affected
Abnormal sensation
Weakness in arms/legs
Bladder/bowel problems
What is spinal shock
Areflexia/hyporeflexia and autonomic dysfunction that accompanies a spinal cord injury
Anterior spinal artery syndrome
This is a syndrome caused by ischaemia of the anterior spinal artery, it results in loss of function of the anterior 2/3rds of the spinal cord
What regions are affected in anterior spinal artery syndrome
Anterior 2/3rds of spinal cord:
Corticospinal tracts
Spinothalamic tract
Autonomic fibres
Features of anterior spinal artery syndrome
Loss of motor function
Loss of pain/touch/temperature sensation
Hypotension
Anterior spinal artery syndrome prognosis
High mortality rate (>20%)
Unsure on treatment
Central cord syndrome
Most common form of cervical spinal cord injury
Characterised by loss of motion and sensation in arms/hands
Tracts affected in central cord syndrome
Corticospinal tract
Causes of central cord syndrome
Trauma
Common in over 50s due to osteoarthritis causing spondylosis (narrowing of spinal cord)
Features of central cord syndrome
Dysproportionately greater motor impairment in upper compared to lower extremities
Variable degree of sensory loss
Bladder dysfunction
Urinary retention
Treatment of central cord syndrome
Immobilisation of the neck
Inpatient physiotherapy
Surgical - cervical spinal decompression
Which organisms cause meningitis?
Neonates:
Group B strep
3-6 months:
N. meningitidis
Strep pneumoniae
6-60 years:
N. meningitidis
Strep pneumoniae
> 60 years:
Strep pneumoniae
N. meningitidis
Immunosuppressed patients:
Listeria monocytogenes
Symptoms of meningitis
Headache Fever Nausea/Vomiting Photophobia Drowsiness Seizures
Signs in meningitis
Neck stiffness
Purpuric rash
Bacterial meningitis and CSF
Cloudy
Glucose: low
Protein: High
White cells: high
Viral meningitis and CSF
Clear/cloudy
60-80% of plasma glucose
Normal/raised protein
Raised lymphocytes
Vaccines against meningitis
Meningitis A, B and C vaccines given 3 times:
2 months
4 months
12-13 months
Investigations in meningitis
FBC CRP Coagulation screen Blood cultures Whole-blood PCR Blood glucose Blood gas LP - if no signs of raised ICP
Antibiotics in meningitis
IV Cefotaxime
+ amoxicillin if aged >50
Can give IV benzylpenicillin instead if meningococcal meningitis
Aciclovir can be given if viral
Can potentially give gentamicin as well (if suspecting listeria)
Additional management in meningitis
Dexamethasone to reduce neuro sequelae
Prophylaxis should be offered to close contacts if meningoccal
What are the potential neurological sequelae of meningitis
Sensorineural hearing loss (most common)
Epilepsy, paralysis
Sepsis, intracerebral abscess
Brain herniation, hydrocephalus
Meningococcal septicaemia
Non-blanching rash
Plus other systemic symptoms (e.g. fever)
Treatment of meningococcal septicaemia
IV cefotaxime
Treat shock etc.
Symptoms of encephalitis
Fever Headache Psychiatric symptoms Seizures Vomiting
Focal symptoms e.g. aphasia
What is aphasia
Impairment of language affecting the production or comprehension of speech
What is the most common cause of encephalitis in adults
Herpes simplex virus 1
How do we investigate encephalitis
CSF - Lymphocytosis, high protein
PCR for HSV
CT - brain changes
MRI
How do we manage encephalitis?
IV aciclovir
Where does HSV encephalitis most commonly affect
Temporal lobes, causing features like aphasia
Glioblastoma multiforme
Most common primary brain tumour, arising from glial cells (astrocytes, oligodendroctyes) - these are fast growing
Imaging of glioblastoma multiforme
Solid tumours
Central necrosis
Rim that enhances contrast
Treatment of glioblastoma multiforme
Dexamethasone treats the oedema
Surgery w/post-op chemo/radiotherapy
Meningioma
The second most common primary brain tumour in adults, it forms on the tissue of the meninges
They are usually benign
Histology of glioblastoma multiforme
Pleomorphic tumour cells border necrotic areas
Histology of meningioma
Spindle cells in concentric whorls with calcified psammoma bodies (calcified collections)
Typical locations of a meningioma
Falx cerebri
Sup. sagittal sinus
Convexity
Skull base
Treatment of meningioma
Usually do a CT with contrast first and MRI
Treatment includes observation, radiotherapy and surgical resection
What is the function of astrocytes?
These are glial cells found in the brain and spinal cord, they help to maintain the blood-brain barrier and aid in the secretion/absorption of neural transmitters
Grading of astrocytoma
WHO grades I to IV
I is least severe, IV is most
Pilocytic astrocytoma
Grade I astrocytoma - a slow growing benign tumour
Can be removed with surgery (stereotactic)
Anaplastic astrocytoma
Grade III astrocytoma
Oligodendroglioma
Benign, slow-growing tumour common in the frontal lobes
Roughly 10% of primary brain tumours
Oligodendroglioma features
Seizure - with frontal lobe activity at onset
Headaches with raised ICP
Histology of oligodendroglioma
Calcifications with ‘fried egg’ appearance
Treatment of oligodendroglioma
Incurable
Watchful waiting
Anticonvulsants and steroids for brain swelling
Ependymoma
Tumour of the ependyma (CNS tissue)
In adults it is often spinal
Common location is in the fourth ventricle
Commonly causes hydrocephalus
Histology of ependymoma
Perivascular psuedorosettes
Symptoms of ependymoma
Raised ICP symptoms: Severe headache Visual loss (papilloedema) Vomiting Drowsiness Gait change
Treatment of ependymoma
Maximum surgical resection followed by radiation
CNS lymphoma treatment
Steroids to reduce swelling/symptoms
Chemotherapy (IV or intrathecally)
What does intrathecally
Into the CNS by lumbar puncture
Cluster headache
Pain, once or twice a day
Each episode lasts 15 mins - 2 hours
Clusters typically last 4-12 weeks
Can have watery eyes
Treatment of cluster headache
100% O2
SC triptan
Verapamil prophylactically
