Neurology Flashcards
Describe the difference between primary and secondary headache
Primary headaches are those where the headache and its associated features are the disorder (i.e. there is no underlying cause), for example; migraine, tension headache, cluster headache
Secondary headaches are secondary to an underlying cause, for example, subarachnoid haemorrhage, space-occupying lesion, meningitis, temporal arteritis etc.
State important features of taking a headache history
Onset (time to maximal symptoms and circumstances at onset)
Severity and Quality of Pain
Location/Radiation of Pain
Presence of Aura/Prodrome
Periodicity (Duration and Frequency)
Associated Features (Photophobia, Nausea, Phonophobia etc)
Age at Onset
Triggers/Exacerbating/Relieving Factors
FHx
Social/Employment Hx
Mediation Hx
Co-Morbid Depression and Sleep Disturbance
State red flag signs and symptoms for headache
Age >50yrs
Thunderclap Headache
Focal/Non-Focal Neurological Deficit
Worsening of Symptoms with Posture, Valsalva or Physical Exertion
Early Morning Headaches
Fever
Weight Loss
Seizures
Meningism
Temporal Artery Tenderness/Jaw Claudication
Specific Situations - Cancer, Pregnancy, Post-Partum, HIV, Immunosuppression
State features of high and low pressure headaches
- Raised Pressure
- Worse on lying flat, in the morning, on Valsalva and physical exertion
- Improved on sitting/standing
- Persistent N/V
- Optic disc swelling, impaired visual acuity, restricted visual fields
- 3rd and 6th CN Palsy
- Caused my mass effect, increased venous pressure, obstruction to CSF flow
- Reduced Pressure
- Worse on sitting/standing
- Relieved by lying down
- Results from CSF leak
Describe the presentation and management of migraine
Triggers include hormones, weather stress, hunger, sleep disturbance, exertion, alcohol excess, foods
Prodrome in up to 60% of patients up to 48 hours before headache (could include mood disturbance, restlessness, hyperosmia, photophobia, diarrhoea)
Aura reported in up to 30% of cases and is a recurrent, reversible focal neurological symptoms (visual, sensory or motor)
Character often throbbing/pulsatile, moderate to severe, unilateral in 60%, gradual onset, lasting 4-72 hours
Associated symptoms include N/V, photophobia, phonophobia, osmophobia, mood disturbance, diarrhoea
Lifestyle management includes avoidance of triggers, reduction of caffeine/alcohol intake, encourage regular meals/sleep patterns
Acute management with simple analgesia, triptans and anti-emetics
Prophylaxis with beta-blockers, TCAs and anti-epileptics
Describe the assessment and investigation of thunderclap headache
‘abrupt onset of severe headache which reaches maximal intensity in <5 mins and lasts >1 hour’
worst headache of my life/like being hit over the head
Causes include SAH, ICH, Arterial Dissection, Cerebral Venous Sinus Thrombosis, Bacterial Meningitis, Primary Headache
Investigate with Bloods, ECG, Urgent CT Head and Lumbar Puncture (after 12 hours)
Describe the pathophysiology of stroke
After stoppage of blood flow to the brain, neurons depolarise within minutes (causing instant onset of early symptoms) and irreversible brain tissue death occurs within 12 hours
Therefore, the sooner the blood flow is restored the more brain death is prevented
Describe the clinical presentation of stroke/TIA
Visual Loss
Weakness
Slurred Speach
Ataxia
Aphasia
Describe the management of stroke
- Ischaemic Stroke
- IV Thrombolysis (within 4.5h) +/- Thrombectomy (within 6-8h)
- Aspirin
- Stroke Unit
- Hemicraniectomy
- Haemorrhagic Stroke
- Aggressive BP Control
- Stroke Unit
- Neurosurgical Evacuation
Define ‘seizure’
‘a transient occurrence of signs and/or symptoms due to abnormal, excessive or synchronous neuronal activity in the brain’
Define ‘epilepsy’
‘a disorder of neuronal activity in the brain defined as two or more unprovoked seizures, or one unprovoked seizure with a lesion in the CNS that increases the probability of a second unprovoked seizure’
Outline the different types of seizure
Focal seizures begin in one part of the brain, and may spread to become secondary generalised
Generalised involves multiple areas of the brain or spread from one area to both sides of the brain
Absence seizures are common in young children
Tonic-Clonic seizures involve LOC and a short tonic phase (muscle suddenly tense and patient falls) and a longer clonic phase (rapid convulsions)
Describe investigations for epilepsy
Diagnosis is largely based on a detailed history from the patient and eyewitness
ECG to check for underlying cardiac problems
EEG is not generally diagnostic but may assist in classification
MRI
Describe the management of epilepsy
- Reduce Pre-Synaptic Excitability
- Voltage Gated Na+ Channel Antagonists
- Carbamazepine
- Lamotrigine
- Voltage Gated K+ Channel Agonist
- Retigabine
- Voltage Gated Na+ Channel Antagonists
- Stops Neurotransmitter Release
- SV2A Vesicle Antagonist
- Levetiracetam
- Voltage Gated Ca2+ Channel Antagonist
- Pregabalin
- Gabapentin
- SV2A Vesicle Antagonist
- GABA-ergic System Agonists
- GABA Metabolism Inhibitor
- Valproate
- Vigabatrin
- GABA Transporter Antagonists
- Tiagabine
- GABA Metabolism Inhibitor
- Reduces Post-Synaptic Excitability
- GABA Receptor Agonist
- Benzodiazepines
- AMPA and NMDA Receptor Antagonist
- GABA Receptor Agonist
Usual treatment for Focal is Lamotrigine, Carbamazepine or Levetiracetam and for Generalised it is Valproate, Levetiracetam and Lamotrigine
Describe the management of Status Epilepticus
‘a single clinical seizure lasting more than 30 minutes or repeated seizures over a period of time greater than 30 minutes without intervening recovery of consciousness’
MEDICAL EMERGENCY
May cause profound systemic/neurological damage if left untreated
Immediate management includes assessing and securing the airway, administering oxygen and assessing pulse, BP and RR
If seizures continue for more than 5 minutes, the seizure should be treated with IV benzodiazepines
If seizures continue, the patient may need sedated and intubated
State causes of loss of consciousness
Epilepsy (Seizures)
Syncope
Stroke/TIA
Drugs
Hypoglycaemia
Alcohol
Hypoxia
Describe the pathogenesis of subarachnoid haemorrhage
Most SAH are caused by aneurysms which form under haemodynamic stress
Extensive inflammatory and immunological reactions are common in unruptured intracranial aneurysm and may be related to aneurysm formation and rupture
A small number (15-20%) are due to other causes. e.g. Arterio-Venous Malformation or Neoplasia
Describe the presentation of subarachnoid haemorrhage
Sudden Onset Thunderclap Headache
LOC
Seizures
Visual, Speech and Limb Disturbance
Sentinel Headache
Photophobia
Meningism
Subhyaloid Haemorrhages
Vitreous Haemorrhages
Pulmonary Oedema
Describe the investigation of subarachnoid haemorrhage
CT - Confirms diagnosis and may give clues to aetiology - Very accurate
LP - For presence of xanthochromia (bilirubin or OxyHb) in the CSF - Conducted at least 12 hours after onset of symptoms
CT/MRI Angiography
Digital Subtraction Angiography
Describe the management of subarachnoid haemorrhage
Bed Rest
Fluids (2.5-3 Litres of Normal Saline)
Anti-Embolic Stockings
Nimodipine
Analgesia
Surgical Clipping (10-15%)
Endovascular Repair (Coils, Stents and Glue) (80-85%)
Describe the complications of subarachnoid haemorrhage
- Rehaemorrhage
- 5-10% incidence in the first 72 hours
- Immediate repair reduces risk
- Delayed Ischaemia
- At Days 3-10
- Progressive deterioration in LOC associated with new deficit
- Managed with fluid resus, nimodipine, inotropes, angioplasty
- Hydrocephalus
- Hyponatraemia
- ECG Changes
- LRTI
- PE
- UTI
- Seizures
- 1-7% of patients
- DVT
- SAH induces a prothrombotic state
Describe the Glasgow Coma Scale
Describe the clinical presentation of radial nerve mononeuropathy
Wrist and Finger Drop
Usually Painless
Motor Weakness; Wrist/Finger Extension and Elbow Flexion in Mid-Pronation
Sensory Change: Radial Part of Dorsum of Hand
Describe the clinical presentation of ulner nerve mononeuropathy
Weak Grip
Usually Painless
Motor Weakness: Index Finger/Pinkie Abduction, Wrist Flexion and Thumb Adduction
Sensory Change: Medial 1.5 Fingers
Describe the clinical presentation of median nerve mononeuropathy
Hx of Intermittent Nocturnal Pain, Numbness and Tingling
Weak Grip
+ve Tinel’s Sign/Phalen’s Test
Motor Weakness: MCP/Thumb Flexion, Thumb Opposition and Thumb Abduction
Sensory Change: Lateral 3.5 Fingers on Palm and Tips of Those Fingers on Dorsum
Describe the clinical presentation of femoral nerve mononeuropathy
Weakness of Quadriceps
Weak Hip Flexion
Numbness in Medial Shin
Motor Weakness: Knee Extension, Hip Flexion, Hip Adduction
Sensory Change: Medial Lower Limb
Describe the clinical presentation of common peroneal nerve mononeuropathy
Acute Onset Foot Drop and Sensory Disturbance
Usually Painless
Motor Weakness: Ankle Dorsiflexion, Great Toe Extension
Sensory Change: Shin and Dorsum of Foot
Describe the epidemiology of multiple sclerosis
UK prevalence of 1.2/1000
More prevalent in Scotland and in northern latitudes
Twice as common in women than men
Describe the pathophysiology of multiple sclerosis
Plaques of demyelinating lesions are the cardinal features of MS
Plaques can occur anywhere in the CNS white matter, however, they have a predilection for distinct sites: optic nerves, the periventricular region, the corpus callosum, the brainstem and its cerebellar connections and the cervical cord
Grey matter of the cortex and the sub-pial meninges are also affected in the early stages however peripheral nerves are not
Acute relapses are caused by focal inflammation causing myelin damage and conduction block and recovery follows as inflammation subsides and re-myelination occurs
In severe damage, secondary permanent axonal destruction occurs which is the pathological basis of the progressive disability in progressive forms of MS
Describe the clinical presentation of multiple sclerosis
Optic Neuritis
Spinal Cord Lesions (Paraparesis, Difficulty Walking, Limb Numbness, Tingling)
Brainstem Demyelination (Diplopia, Vertigo, Facial Numbness/Weakness, Dysarthria, Dysphagia)
Visual Change, Sensory Symptoms, Clumsy Hand or Limb, Unsteadiness, Ataxia, Urinary Symptoms, Pain, Fatigue, Spasticity, Depression, Sexual Dysfunction, Temperature Sensitivity
Describe the investigation of multiple sclerosis
MRI Brain and Spinal Cord - To investigate for demyelinating lesions
Bloods to exclude other inflammatory conditions such as Sarcoidosis and SLE
Visual Evoked Response
LP - IgG Oligoclonal Bands in 85-90%
Describe the main subtypes of multiple sclerosis
- Relapsing Remitting
- Unpredictable attacks which may or may not leave permanent deficits followed by periods of remission
- Primary Progressive
- Steady increase in disability without attacks
- Secondary Progressive
- Initial relapsing-remitting pattern that suddenly begins to decline without periods of remission
- Progressive Relapsing
- Steady decline from onset with super-imposed attacks
Describe the pathology of Parkinson’s Disease
Loss of dopaminergic neurones within substantia nigra
PD manifests clinically after loss of approximately 50% of dopaminergic neurons
Surviving neurones contain Lewy Bodies (aggregates of misfolded proteins in the cytoplasm)
Progresses from Stage 1/2 (Medulla/Pons), to Stage 3/4 (Midbrain, Substantia Nigra, Pars Compacta - Parkinsonism) to Stage 5/6 (Neocortex - PD Dementia)
Describe the clinical features of Parkinson’s Disease
Bradykinesia, Muscular Rigidity, Postural Instability, 5-6Hz Rest Tremor
Dementia, Depression, Anxiety
Constipation, Urgency, Nocturia, Erectile Dysfunction, Excessive Salivation, Postural Hypotension, Sweating
REM Sleep Behaviour Disorder, Restless Leg Syndrome, Daytime Somnolence
Reduced Olfactory Function, Fatigue, Pain and Sensory Symptoms
Describe the differential diagnosis of Parkinson’s Disease
Benign Tremor Disorders (e.g. Essential Tremor)
Dementia with Lewy Bodies
Vascular Parkinsonism
Parkinson Plus Disorders
Drug Induced Parkinsonism/Tremor
Describe the pharmacological management of Parkinson’s Disease
- L-Dopa
- Taken up by dopaminergic neurones and decarboxylated to dopamine within presynaptic terminals
- Adverse effects include nausea, vomiting and postural hypotension (peripheral) and confusion and hallucinations (central)
- Prescribed with a dopa-carboxylase inhibitor
- Dopamine Agonists
- e.g. Ropinirole, Pramipexole
- Acts directly on post-synaptic striatal dopamine receptors (D2)
- Longer half-life, lower efficacy but fewer motor complications than L-Dopa
- MAO-B Inhibitors
- e.g. Selegiline, Rasagiline
- Prevents dopamine breakdown by binding irreversible to monoamine oxidase
- COMT Inhibitors
- e.g. Entacapone, Tolcapone
- Inhibiting COMT results in longer L-Dopa half-life/duration of action
Describe Myasthenia Gravis
Autoimmune disorder with auto-antibodies to acetylcholine receptor at post-synaptic neuromuscular junction
Association with other autoimmune disorders
May be associated with thymic hyperplasia or thymoma
Affects young women in 20’s and older men in 70’s
Causes fatigable weakness of ocular, bulbar, neck, respiratory and/or limb muscles
Investigated with antibodies to AChR (present in 85% of cases) and abnormal single fibre EMG
Managed with Pyridostigmine (anti-acetylcholine esterase) and immunosuppressive therapies (e.g. steroids and intravenous Immunoglobulin)
Describe the pathogenesis and clinical presentation of length-dependent axonal neuropathy
Most common cause in the western world in Diabetes Mellitus
Severely damaged axons degenerate distally
Within a week the nerve becomes electrically inert
Muscle fibres supplied by damaged motor nerves atrophy
EMG records show fibrillation potentials
Undamaged motor fibres sprout to supply more muscle fibres
Demyelination:
Demyelination of peripheral nerve fibres initially leaves the axon intact
The result is blockage or slowing of conduction
Pressure or entrapment neuropathies are primarily caused by demyelination
Inflammatory processes e.g. Guillain-Barre are caused by demyelination
Presents with tingling, numbness and in the peripheries, typically in a gloves and stocking pattern
Describe the pathology of common dementias
Alzheimer - Generalised atrophy, beta-amyloid plaques and neurofibrillary tangles
Vascular - Strokes, lacunar infarcts and white matter lesions
Lewy Body - Generalised atrophy with lew bodies in the cortex and midbrain
Frontotemporal - Frontotemporal atrophy and pick cells/bodies in the cortex
Describe the clinical presentation of common dementias
Alzheimers - Memory loss, aggression, language deficit, impaired visuospatial
Vascular - Focal neurological deficits, evidence of vascular disease
Lewy Body - Fluctuating cognition, visual hallucinations, shuffling gait, increased tone, tremors
Frontotemporal - Disinhibition, socially inappropriate behaviours, poor judgement and cognitive function
Describe the investigation of common dementia syndromes
All patients should have a routine dementia screen, including FBC, U&Es, LFTs, TFTs, Glucose, VitB12 and Folate
Cognitive function should be assessed using the Mini Mental State Exam (
Describe the management of Multiple Sclerosis
Education from an MS Nurse Specialist
Immunisations (avoid live vaccines if on disease-modifying drugs)
Early management of infections
Symptomatic treatment (e.g. pain, spasticity and urinary features)
Physiotherapy/Occupational Therapy
Short courses of steroids such as IV Methylprednisolone for 3 days (or high dose oral steroids) are used for severe relapses
