Neurology Flashcards
Emergencies
How is coma measured?
On the Glascow Coma Scale
Emergencies
What are criteria for a coma?
GCS <8
Emergencies
List the eye responses and their grading on the GCS
- No eye opening
- Opens to painful stimulus
- Opens to voice
- Spontaneously open
Emergencies
List the voice responses and their grading on the GCS
- No speech
- Incoherent speech
- Inappropriate words
- Confused
- Orientated
Emergencies
List the motor responses and their grading on the GCS
- No movement
- Extending
- Flexing
- Withdraws from painful stimulus
- Localises to painful stimulus
- Obeys commands
Emergencies
What are the common causes of coma?
Drugs, toxins (opiates, alcohol)
Head injury
Metabolic (Hypoglycaemia, DKA, hepatic encephalopathy, uraemia)
Seizures
Anoxia (post arrest)
Mass lesions (bleeds, abscess)
Infections (HSE, bacterial meningitis)
Infarcts (brainstem)
SAH
Neurology
What might purposeful eye movement indicate in a patient who is otherwise unresponsive?
A psychogenic cause e.g., catatonia or locked-in syndrome
Neurology
What might blood or clear fluid in the ears indicate in an unresponsive patient?
Blood or leakage of CSF in the ears can indicate a fracture at the base of the skull
Neurology
What may periorbital bruising or bruising around the mastoid process indicate in a patient who is unresponsive?
Basilar skull fracture
Neurology
What investigations should be performed for a patient that has reduced GCS?
Depending on suspected causes
Basic bloods including glucose (FBC, U&E, LFTs)
If indicated:
* ABG
* Imaging (CT or MRI)
* Lumbar puncture
* EEG
* Toxilogy and alcohol levels
Neurology
How does herpes simplex encephalitis present?
Affects temporal lobes
* Fever
* Headache
* Psychiatric symptoms
* Seizures
* Vomiting
* Focal features e.g., aphasia
Neurology
What investigations should be performed for suspected herpes simplex encephalitis?
CSF: lymphocytosis, high protein
PCR for HSV
CT: medial temportal and inferior frontal changes, no changes in a third of patients
MRI more reliable
EEG: lateralised periodic discharges at 2Hz
Neurology
What is the treatment for herpes simplex encephalitis?
IV aciclovir
Neurology
What is status epilepticus?
Seizure lasting:
* 5 minutes for generalised tonic-clonic seizures
* 10 minutes for focal seizures
* 10-15 minutes for absence seizures
Neurology
What are the complications of status epilepticus?
- Increased CNS metabolic consumption
- Rhabdomyolysis
- Renal failure
- Metabolic acidosis
- Hyperthermia
- Heart and other organ effects
- End organ damage due to lack of oxygen
Neurology
What is the management of status epilepticus?
- Benzodiazepam if fitting >5mins
- Second dose of benzodiazepam after 10 minutes
- Phenytoin or levetiracetam or sodium valproate + inform ICU
- General anaesthesia with intubation and ventilation
Neurology
How does third nerve palsy present?
Ptosis with diplopia on upward gaze
Eye deviated ‘down and out’
Pupil may be dilated
Neurology
What is associated with sudden onset headache + CN III palsy OR painful CN III palsy?
Sub-arachnoid haemorrhage
Neurology
What are the causes of SAH?
Most commonly ruptured saccular aneurysms
Non-aneurysmal:
* trauma
* cranial or spinal vascular malformations
* dissection of an intracranial artery
* illicit drug use
* cerebral venous thrombosis
Neurology
How does SAH present?
- ‘Thunderclap’ headache - within one minute, very severe
- Transient loss of consciousness
- Vomiting
- Meningism (neck pain or stiffness)
- Altered neurology, seizures or focal neurological deficit
- Sentinel headache (previous sudden severe headache)
- O/E: CN III palsy, subhyaloid haemorrhage, may have bilateral extensor plantar responses
Neurology
What investigations should be performed for SAH?
CT head
CT angiogram or MRI/MR angiogram
Lumbar puncture 12 hours after the event - high red cell count,
Neurology
What is an aneurysm?
Ballooning at a weak spot in an artery wall
Neurology
What is the investigation for aneurysms?
Angiography
Neurology
What is the definitive management of aneurysms?
Endovascular coiling or neurosurgical clipping
Neurology
How does Guillian-Barre syndrome present?
- acute or subacute
- demyelinating > axonal
- immue-mediated, post infectious (resp or GI common)
- multifocal polyradiculo-neuritis
- numbness starts distally
- progressive ascending weakness
- bifacial weakness and other cranial neuropathies
- flaccid tetra/para paresis
- areflexia
Neurology
How is Guillian-Barre syndrome diagnosed?
CSF: cyto-protein dissociation/pleocytosis, elevated protein, few or no cells
EMG: slow nerve conduction velocities
Neurology
What are the complications of Guillian-Barre syndrome?
Severe weakness
Aspiration
Respiratory failure
Autonomic instability: major cause of death, severe sudden hypotension and cardiac arrhythmia
Neurology
How is Guillian-Barre syndrome managed?
- Hospital admission
- ITU care: <1 vital capacity OR sniff pressures, counting in one breath
- DVT prophylaxis
- BP
- ECG
- Monitor swallow: NG feeding may be needed
- Treatment: IV Ig or plasma exchange
Neurology
How does an upper motor neurone lesion present on examination?
Bulk: normal
Tone: increased
Strength: decreased
Fasculations: absent
Reflexes: increased
Neurology
How does a lower motor neurone lesion present on examination?
Bulk: reduced (wasting)
Tone: normal or decreased
Strength: decreased
Fasciculations: may be present
Reflexes: decreased or absent
Neurology
How is damage to the peripheral nerves classified?
Polyneuropathy
Mononeuritis multiplex: at least two nerves
Mononeuropathy: one single nerve
Neurology
How does polyneuropathy present?
Affects peripheral nerves
Usually chronic and slowly progressive
Starts in the legs and longer nerves
Sensory, motor or both
Neurology
What causes peripheral neuropathy with predominantly motor loss?
- Guillian Barre syndrome
- Chronic Inflammatory demyelinating polyneuropathy (CIDP, chronic version of GBS)
- Hereditary sensorimotor neuropathies (HSMN) e.g., Charcot-Marie-Tooth disease
- Diptheria
- Porphyria
Neurology
What causes peripheral neuropathy with predominantly sensory loss?
Deficiency states e.g., B12/folate
Diabetes
Alcohol/toxins/drugs
Metabolic abnormalities e.g., uraemia
Leprosy
Amyloidosis
Neurology
What is mononeuritis multiplex and how does it present?
Painful, asymmetrical sensory and motor neuropathy
* Subacute presentation
* Inflammatory/immune mediated
Neurology
What are the causes of mononeuritis multiplex?
Vasculitides e.g., Churg Strauss
Connective tissue disorders e.g., Sarcoid
Neurology
What are some examples of mononeuropathy?
Median nerve entrapment at the wrist (carpal tunnel syndrome)
Ulnar nerve at elbow
Radial nerve in axilla
Common peroneal nerve in leg
Neurology
What investigations should be performed for neuropathy?
Neuropathy screen: FBC, ESR, U&E, glucose, TFT, CRP, serum electrophoresis, B12, Folate, Anti-Gliadin, TPHA, HIV
Vasculitic screen: FBC, ESR, U&E, Creatinine, CRP, ANA, ANCA, anti dsDNA, RhF, complement, cryoglobulins
EMG/NCS
CSF study
Imaging/nerve biopsy
Neurology
What is the management of neuropathy?
- 20% idiopathic - neuropathic analgesia (gabapentin, pregabalin, amitriptyline)
- Treat/remove underlying cause
- Inflammatory: prednisolone with steroid sparing agents e.g., azathioprine
- Vasculitic: prednisolone with immunosuppresant e.g., cyclophosphamide
Neurology
What is myasthenia gravis?
An autoimmune disorder, antibodies against nicotinic acetylcholine receptors
Neurology
How does myasthenia gravis present?
- More common in women
- Muscle fatigability - progressively weaker after activity and improves with rest
- Extraocular muscle weakness: diplopia
- Proximal muscle weakness: face, neck, limb girdle
- Ptosis
- Dysphagia (bulbar symptoms) - especially in elderly
- Proximal limbs weakness
Neurology
What conditions is myasthenia gravis associated with?
Other autoimmune diseases e.g., thyroid, pernicious anaemia, rheumatoid, SLE
Thymomas in 15%
Thymic hyperplasia in 50-70%
Neurology
What investigations should be performed for myasthenia gravis?
Tensilon test: allow accumulation of ACh in the neuromuscular junction
AChR antibodies
EMG (single fibre)
CT thorax to exclude thymoma
Creatinine kinase: normal
Neurology
How is myasthenia gravis managed?
If symptomatic: acetylcholine esterase inhibitors (pyridostigmine)
Immunosuppresants: steroids, azathioprine/methotrexate/mycophenolate
Thymectomy
Neurology
What is myasthenic crisis?
Severe weakness including respiratory muscles
Neurology
What are the causes of myasthenic crisis?
Infection
Natural cycle of disease
Under-dosing or overdosing of medication
Neurology
What is the management of myasthenic crisis?
Urgent review by neuro
ABCDE, monitor breathing
Anaesthetist review
Plasmapherisis
IV Ig
Neurology
What is motor neurone disease?
Degeneration of motor neurons in the motor cortex and anterior horns of the spinal cord
Neurology
How does motor neurone disease present?
- Both upper and lower motor neurone symptoms
- fasciculations
- absence of sensory signs/symptoms
- wasting of small hand muscles/tibialis anterior
- not affecting external ocular muscles
- no cerebellar signs
- asymmetric weakness
- no visual involvement
- bulbar or limb onset
Neurology
What investigations should be performed when MND is suspected?
Clinical diagnosis, investigations rule out other conditions
LP
NCS/EMG
MRI
Neurology
What are some examples of common muscle disorders?
Steroid myopathy
Statin myopathy
Metabolic and endocrine myopathies
Myotonic dystrophy
Neurology
What are some examples of uncommon muscle disorders?
Most muscular dystrophies: Duchenne, Becker, Facioscapulohumeral
Inflammatory muscle disease: Polymyositis, dermatomyositis
Mitochondrial disorders
Neurology
How do muscle disorders present?
- Stairs, chairs and hairs
- Wasting
- Facial weakness in some e.g., facioscapulohumeral dystrophy
- Neck weakness
- Contractures
- Scoliosis especially in Duchenne
- Eye movement disorders rare, seen in mitochondrial disorders
Neurology
What investigations should be performed for muscle disorders?
Creatinine kinase
EMG
ESR/CRP
Genetics
Biopsy
Neurology
What is the management of muscle disorders?
Remove causal agent
Supportive: occupational therapy, physio, back, renal, diet
Immunosuppress if inflammatory
Blackouts
How does syncope present?
Before:
* prodrome/precipitant/posture
* minor warning
* standing/hot room/vagal maneuvers
* looked grey/sweaty/clammy
* chest pain/exertion
* sudden startle in long QT syndrome
During:
* rapid onset
* minimum twitching
After:
* rapid recovery
* no confusion
Others:
* previous events
* known low BP
* cardiac drugs
* drugs that cause ECG changes
* family history of cardiac disease
Blackouts
How does vasovagal syncope present?
Triggered by pain, prolonged standing, emotional stress, instrumentation
Blackouts
How does situational syncope present?
Micturition, swallow, defecation, cough, sneeze, post-exercise, laughing
Blackouts
How does carotid sinus syndrome present?
Loss of consciousness while turning head to one side, particularly in men >50 years old
Blackouts
What is orthostatic hypotension caused by?
Drug induced: vasodilators, diuretics, phenothiazine, antidepressants
Volume depletion: haemorrhage, diarrhoea, vomiting
Primary autonomic failure/neurogenic: pure autonomic failure, multiple system atrophy, Parkinson’s, dementia with Lewy bodies
Secondary autonomic failure/neurogenic: diabetes, amyloidosis, spinal cord injuries, auto-immune autonomic neuropathy, paraneoplastic autonomic neuropathy, kidney failure
Other causes: adrenal insufficiency, cardiac impairment, vasodilation
Blackouts
How does epilepsy present?
Before:
* no precipitant
* from sleep/sleep deprivation/alcohol withdrawal
During:
* no warning/aura
* posturing of limbs, head turning, eye gaze, groaning/grunting
* tonic then clonic
* very rhythmic shaking then gradually eases off
* no stopping and starting
* short duration <5mins
* eyes open, gaze may be deviated
After:
* confused
* tongue biting, incontinence urine and faeces
Other:
* brain injury/illness
* minor seizures
* family history of epilepsy
Blackouts
How does non-epileptic attack disorder present?
Before:
* precipitant (often repeated)
* prodrome (patient can’t describe)
During:
* may collapse or shake
* may be prolonged up to 45mins
* wax and wane
* inconsistent
* irregular
* respond during attack
* vary in features
* eyes closed/resisting opening
After:
* quick or slow recovery
* may be emotional
Other:
* patient unable to describe attack but able to describe consequences
Blackouts
What investigations should be performed for loss of consciousness?
BP lying/standing
heart sounds
ECG
If cardiac suspected: prolonged ECG and echo
If epilepsy suspected: MRI and/or EEG
Blackouts
What is the management of syncope?
Vasovagal: advice
Orthostatic: review drugs, advice, compression stockings, raise head of bed
Blackouts
What is the management of NEAD?
Explanation/advice/support
Psychotherapy
