Neurology Flashcards
Definition of Migraine & Types
A primary headache disorder, form of sensory processing disturbance with manifestations within & outside CNS function
A recurrent, moderate to severe headache commonly a/w nausea, photophobia & phonophobia.
The headache is typically unilateral and pulsating in nature lasting 4-72 hours.
There are two major types of migraine:
- Migraine without aura: characteristic migraine headache with associated symptoms.
Migraine with aura: a migraine headache that is preceded (and sometimes accompanied) by focal neurological symptoms.
Possible triggers/risk factors for Migraine
Stress Caffeine intake Menstruation Exercise Lack of Sleep OCP Certain foods e.g. chocolate Family history
Clinical features of Migraine
Unilateral or bilateral throbbing/pulsating headache Can be preceded by an aura Visual changes Moderate to severe pain a/w nausea, photophobia, phonaphobia wanting to sleep/sit in dark quiet room
Management of Migraine
Preventative measures - avoid triggers, keep diary, lifestyle advice
Acute - NSAID e.g. aspirin at aura, triptan at headache (sumatriptan), antiemetic e.g. metoclompromide
Preventative (if >2/month) - beta blockers, amitriptyline, topiramate, candasartan
Definition of Cluster Headaches
A severe primary headache disorder characterised by recurrent unilateral headaches centred on the eye or temporal region.
Clinical Features of Cluster Headaches
Unilateral severe headache
Autonomic sx – eye streaming, runny nose, conjunctival congestion, swelling of face/eyelids
Some patients can have night time attacks which will wake pt from sleep usually 2-6am
Severe agitation & restlessness
Periodicity
Investigations & Diagnosis of Cluster Headaches
Investigations:
Patients presenting with their first bout of a cluster-like headache should be referred to neurology for further review.
• Due to TACs being v common, patients should be referred to neurology as dx should be confirmed by specialist
Investigations typically consist of imaging to exclude sinister causes:
• MRI Brain
• CT Head
Diagnosis - clinical, dx by specialist
Management of Cluster Headaches
Aim to terminate acute attacks & prevent further ones
• Sumatriptan is often used first-line to terminate acute attacks (S/C or intranasally)
• Short burst oxygen therapy: 100% oxygen (12-15L/min) can be administered via a non-rebreather face mask for 15-20 minutes
• Avoid triggers e.g. alcohol, smoking
Traditional analgesic medications like paracetamol, opiates and NSAIDs are not recommended.
Preventative (long term) - verapamil (high dose, ECG monitoring), topiramate
Definition of Trigeminal Neuralgia & Clinical Features
Sudden, severe facial pain, often described as a sharp shooting pain or like having an electric shock in the jaw, teeth or gums (within the distribution of the trigeminal nerve).
Short-lived episodes of electric shock pain in the distribution of the trigeminal nerve
Usually unilateral (>97%)
Recurrent attacks - triggers inc cold air, eating
Aetiology of trigeminal neuralgia
Primary trigeminal neuralgia
• Refers to disease caused by vascular compression - thought to account for 80-95% of cases
• This normally occurs near the root of the nerve at the ‘nerve root entry zone’
• The compression is thought to lead to demyelination and abnormal electrical activity in response to stimuli
Secondary trigeminal neuralgia
• Refers to disease occurring secondary to another condition
• Compression may be caused by other lesions (e.g. vestibular schwannoma, meningioma, cysts)
• Multiple Sclerosis
Idiopathic trigeminal neuralgia
Management of Trigeminal Neuralgia
Consider urgent ref for MRI if sinister cause suspected
1st line - carbamazepine 100mg BD & titrate upwards until remission
2nd line - gabapentin or lamotrigine
Surgical options - microvascular decompression or gamma knife radiosurgery
Definition & Risk factors for Idiopathic intracranial hypertension
A disorder caused by chronically elevated intracranial pressure (ICP), which leads to the characteristic clinical features of headache, papilloedema (swollen optic discs) and visual loss.
Weight (obesity), age (reproductive age) & sex (female)
Clinical features of IIH
Headache - worse on lying down, bending forwards & in the morning
Visual changes - transient vision loss, flashes of light, diplopia
Tinnitus
Neck/back pain
pain behind eyes
papilloedema
6th nerve palsy
Investigations for IIH
Obs (BP) Urinalysis - pregnancy & renal disease Bloods Opthalmoscopy MRI (R/O other causes) LP - measure pressures
Differentials for IIH
SOL, venous sinus thrombosis, obstructive hydrocephalus, decreased CSF reabsorption or increased CSF production
Management of IIH
Weight loss
• Low sodium weight loss plan
Serial LPs
Occasionally may be offered to remove excess CSF
Pharmacotherapy
• carbonic anhydrase inhibitor (e.g. acetazolamide) is the treatment of choice for IIH
• Thought to work by reducing amount of CSF production
Surgical
• Optic nerve sheath fenestration
Shunting
Clinical Features of Tension Type Headache
Classically they produce a mild ache across the forehead and in a band-like pattern around the head.
This may be due to muscle ache in the frontalis, temporalis and occipitalis muscles. Tension headaches comes on and resolve gradually and don’t produce visual changes.
Risk factors/associations for tension type headaches
Stress Depression Dehydration Alcohol Skipping meals
Red Flags in Headaches
Headache Characteristics - severe sudden onset, progression or acute changes, worse on standing/lying down
Precipitating factors - recent trauma (subdural), triggered by Valsalva manoeuvre
Associated features -
fever/photophobia/neck stiffness (meningitis), papilloedema (IIH, SOL, CVS), vomiting (SOL, CO poisoning), dizziness/vertigo (stroke), visual changes (GCA, glaucoma)
Patient factors - age >50 or <10, immunodeficiency, active or previous cancer, pregnancy
Management of Tension Headaches
Analgesia: Simple painkillers such as paracetamol of NSAIDs (if no contra-indications), to be taken when headache occurs.
Lifestyle: Evaluate and offer help with possible precipitants. Consider sources of stress, depression/anxiety, sleep disorder and chronic illnesses. Some patients find regular exercise helps.
Medication-Overuse Headaches; definition & management
Medication ‘overuse’ itself has been shown to result in chronic headaches.
As the name suggests this occurs when regular analgesia taken for symptomatic relief of headache causes or perpetuates the condition.
It gives similar non-specific features to a tension headache.
Stop/reduce medications within a month - may get worse before better
Definition & Aetiology of Subarachnoid Haemorrhage
Arterial haemorrhage/bleeding into subarachnoid space (bet arachnoid & pia mater)
Traumatic - HI
Spontaneous - aneurysm rupture, AVM, rarer (CA dissection)
Risk factors for SAH
Hypertension
Smoking
Alcohol
Substance/drug abuse e.g. cocaine, amphetamines
Sex - higher risk in females
Race: higher incidence in Japanese/Finnish populations
Family history of aneurysms
Genetic predisposition
○ autosomal dominant polycystic kidney disease (increased tendency to form berry aneurysms) or type IV Ehlers-Danlos syndrome
Clinical features of SAH
Sudden severe thunderclap headache Photophobia & neck stiffness N&V Visual changes - ptosis, 3rd nerve palsy, diplopia Reduced GCS
Investigations & Management of SAH
Observations & Examination, Bloods inc G&S, clotting, Imaging (CT head)
If CT head normal - LP in 12hrs (detect bilirubin)
Initial management - A to E survey, ?airway management if needed
Medical - analgesia, anti-emetics, IV fluids & monitoring, regular neurological observations, nimodipine
Surgical/aneursym management - coiling/clipping
Definition & Aetiology of Subdural Haemorrhage
Rupture of bridging veins, bleeding between dura & surface of brain
acute - within 72hrs, subacute 3-20days, chronic after 3 weeks
Usually caused by trauma (fall, HI) but can be caused by aneurysm rupture, AVM etc
RFs: elderly, alcoholics, anticoagulated, HTN, presence/hx of aneurysms
Clinical features of Subdural Haemorrhage
History of trauma & HI with decreased level of consciousness (ACUTE)
Worsening headaches for 7-14days after injury, altered mental state (SUBACUTE)
Headache, fluctuating confusion, cognitive impairment, focal weakness, seizures (CHRONIC)
Seizures Weakness Vomiting Reduced consciousness Sudden neurological sx
Investigations for subdural haemorrhage
Urgent CT head - confirm diagnosis, crescent shaped
• History/examination/observations - inc neuro examination, pupils & A-E survey
• Bloods - FBC (Hb, plt), U&Es, LFTs (alcohol), clotting, G&S, bone profile
• Imaging - CT head
○ Crescent shaped
○ Acute subdural bleeds = hyperdensity = paler
Chronic subdural bleeds = hypodense = darker
Management of Subdural Haemorrhage
Management:
Initial
A to E survey; C spine, D inc pupil check & GCS, signs of raised ICP
Conservative
If small & minimal midline shift
Closely monitor with neuro obs, manage & prevent ICP
Ensure normal sats, normal temp, normal CO2, adequate sedation and paralysis, ICP monitoring
Seizure management
Surgical
Stopping bleeding/evacuation of chronic subdurals
Burr Holes
Definition & Aetiology/RFs - Extradural Haemorrhage
Bleeding into extradural space - above dura mater
Trauma - high impact, high energy trauma
Causes temporal/parietal bone fracture which leads to damage/tear of MMA
Mechanism of Injury Anticogulation/antiplatelet use Alcohol excess Liver dysfunction Coagulopathy
Clinical Features - Extradural Haemorrhage
· History of trauma, brief LOC followed by a lucid interval · Headache · Nausea & vomiting · Seizures Speech difficulties
• Reduced GCS/consciousness • Confusion • Focal neuro deficits • Unequal pupils • Herniation CSF leak
Investigations for Extradural Haemorrhage
Plain CT head - shows blood in extradural space, forms lemon shape, midline shift
• Bedside; neuro obs & examination, history, BM & ECG
• Bloods; FBC (Hb, plt), U&Es, LFTs (alcohol), clotting, G&S, CM, bone profile
Imaging; CT head +/- full trauma screen e.g. whole body CT
Management of Extradural Haemorrhage
Trauma call & primary survey Any resuscitation that is appropriate Admit to HDU Discuss with specialist neuro team Surgery - decompression
Definition & Types of Multiple Sclerosis
Chronic, immune mediated, neuroinflammatory condition which involves demyelination of central nervous system (UMN)
Relapsing-remitting
Primary progressive MS
Secondary progressive ms
Risk factors/aetiology - MS
• Genetics
○ Increased risk if family hx
○ Twins - 1 in 5, if identical twin is affected –> shows GxE
• Vit D levels
○ Live further away from the equator = increased risk
○ Patients with MS have lower Vit D levels - ?cause vs effect
○ Some genetic components linked to development of MS & involved in Vit D
• Viral - EBV prevalance
• Obesity
Sex - female
Clinical features of MS
Visual Symptoms • Optic neuritis - unilateral deterioration visual acuity & colour perception, pain on eye movement • Blurred vision Motor symptoms + UMN symptoms on examination • Limb weakness • Spasms • Stiffness & heaviness Sensory symptoms • Pins & needles • Numbness • Burning Autonomic • Urinary urgency • Hesitancy • Incontinence • Impotence
Management of MS
• Acute attacks - high dose steroids e.g. Methylprednisolone 500mg PO for 5/7
○ Although will get better on own, steroids quicken recovery
Preventing relapses - beta interferon, DMARDs
Definition of Parkinson’s Disease
Neurodegenerative disease - loss of DAnergic neurones within substantia nigra (basal ganglia)
Clinical Features of Parkinson’s Disease
Bradykinesia, rigidity, resting tremor & postural instability
Mask-like expression, micrographia, shuffling gait, gabellar tap
Genetic Factors in Parkinson’s Disease
SNCA DJ-1 - support/chaperone LRRK2 - mutations inhibit autophagy PINK1 PARKIN
Investigations & Diagnosis - Parkinson’s Disease
Clinical diagnosis - history & examination
DX by specialist using criteria
DAT scan - reduced
MRI/CT - r/o other pathologies
Bloods - serum ceruloplasmin to r/o Wilson’s Disease in young onset
Levodopa trial
Differentials for Parkinson’s Disease
Essential tremor - intention tremor, symmetrical
Progressive supranuclear palsy
Multiple systems atrophy - autonomic sx
Dementia with Lewy Body - LBD cognitive symptoms within one year of motor features.
Management of Parkinson’s Disease
Medical - symptomatic therapy with DA replacement
• L-DOPA - levodopa + carbidopa (peripheral DOPA decarboxylase inhibitor)
• DA agonists - ropinirole
• MAO inhibitors - selegiline
• COMT inhibitors - entacapone
Surgical
• Deep Brain stimulation
Defintion/Criteria for Epilepsy
A chronic neurological disorder which is characterised by recurrent seizures
Criteria 1: ≥2 unprovoked (or reflex) seizures occurring more than 24 hours apart
Criteria 2: 1 unprovoked (or reflex) seizure with a probability of further seizures felt to be at a similar recurrence risk to patients with ≥2 unprovoked seizures over the next 10 years.
Criteria 3: A diagnosed epilepsy syndrome
Classification of Epilepsy
Based on seizure type, epilepsy type & syndrome
Seizure type - onset(focal/generalised), awareness, clinical features
Epilepsy type - focal, generalised, both or unknown
Syndrome - can be classified into syndromes based on further findings e.g. onset age, EEG findings
Risk factors for Epilepsy
• Cerebrovascular disease
• Head trauma
• Cerebral infections
• Family history: epilepsy or neurological illness
• Premature birth
• Congenital malformations of the brain
Genetics conditions associated with epilepsy
Differentials - epilepsy mimics
syncope, pseudoseizures, migraine associated disorders, paroxysmal movement disorders, sleep disorders
Investigations for Epilepsy
- ECG
- Bloods: FBC, U&E, LFT, Glucose, Bone profile
- Other: depending on suspected aetiology and age of presentation
- EEG
- MRI Brain
Management of Epilepsy & Important Considerations
Patient Education & Safety
Anti-epileptics - focal (lamotrigine-carbamazepine), generalised (sodium valproate - lamotrigine)
Other options inc: Levetiracetam, Phenytoin
- women of child bearing ages - sodium valproate
- interactions of contraception - CYPP450
Definition of Status Epilepticus
Continuous epileptic activity which failed to self terminate - lasting >5mins
In SE there is prolonged seizure activity either due to failure of the mechanisms responsible for seizure termination, or from the initiation of mechanisms which lead to abnormally prolonged seizures
Causes of status epilepticus
® Part of epilepsy syndrome ® Hypoglycaemia ® Infection (meningitis/ encephalitis) ® Intracranial haemorrhage ® Electrolyte imbalance (hypo/hyper Na+, Ca2+) ® Drug-related · withdrawal – benzodiazepines, opioids · toxicity – tricyclic antidepressants
Management of Status Epilepticus
· Pre-hospital: PR Diazepam (10-20mg) repeat 15mins if continuing or give buccal midazolam 10mg
· Primary survey; protect airway, breathing & circulation
· Check glucose & respond accordingly
Next steps: IV lorazepam phenytoin infusion GA
General principles of management (for us)
® ABCDE
® 2x Benzodiazepines + Call a senior doctor
® Phenytoin / phenobarbitone
Rapid sequence induction
Definition & Types of Encephalitis
Inflammation of brain parenchyma
Infectious - viral (HSV), bacterial, fungi
Non-infectious - AI, paraneoplastic & post infectious
Aetiology of Encephalitis
• Infectious (common) ○ Herpes Simplex Virus (HSV) ○ Others include: arboviruses (e.g. West Nile virus), varicella-zoster virus, Epstein-Barr virus, and human immunodeficiency virus (HIV) ○ Bacterial causes - mycoplasma, TB ○ Fungi - histoplasmosis ○ Parasites
• Non-infectious ○ Paraneoplastic ○ Post-infectious ○ Auto-immune (NMDA & VGKC)
Clinical features of encephalitis
Classic presentation - new onset fever, headache & altered mental state +/- focal neurological deficits
Can be highly variable dependent on underlying cause & area of brain that was been affected
fever, headache, seizures, altered mental status, behavioural changes
Investigations for encephalitis
• Bedside - observations, urinalysis, ECG & sputum cultures
○ Mostly to r/o other causes of infection e.g. UTI
• Bloods - FBC, U&Es, bone profile, LFTs, CRP, cultures & coagulation
• Imaging - CXR & CT head/MIR
r/o stroke, SOL
More specialist: • Neuroimaging • EEG • CSF analysis (Lumbar Puncture) - CT first if worried about SOL Serological testing - antibodies
Management of encephalitis
Principle treatment of HSV encephalitis is IV aciclovir
* HSV encephalitis --> IV aciclovir * Antimicrobials or antivirals directed to cause * Immunosuppressive therapies (e.g. steroids) can be used to treat paraneoplastic, autoimmune, and post-infective causes but it is essential an infection is excluded before these are initiated.
Definition & Pathophysiology of Guillian Barre Syndrome
Acute inflammatory demyelinating polyneuropathy affecting PNS - progressive &ascending
Immune mediated
Aetiology of Guillian Barre Syndrome
• Idiopathic (40%)
• Post-infection (1-3 weeks)
○ Bacterial - campylobacter jejuni most common identifiable trigger
○ HIV
○ Herpes Simplex
• Malignancy (lymphoma, Hodgkin’s Disease)
Clinical Features of Guillian Barre Syndrome
Progressive symptoms of <1mth duration of:
- Ascending symmetrical limb weakness (lower>upper)
- Ascending paraesthesia
May have a history of recent illness e.g. D&V, gastroenteritis
Examination: Motor - hypotonia, flaccid paralysis, areflexia
Sensory - impaired in multiple modalities
Differentials for Guillian Barre Syndrome
Differentials: Lyme disease, sarcoidosis, thiamine deficiency, porphyria and neoplasms
Investigations for GBS
The diagnosis of GBS is suspected based on the clinical presentation. Investigations aim to confirm a diagnosis of GBS and exclude differentials.
Specialist investigations needed: lumbar puncture & nerve conduction studies
Management of Guillian Barre Syndrome
Acute: high dose IV immunoglobins or plasmapheresis may reduce duration or severity
Supportive: airway & cardiac monitoring, DVT prophylaxis, long term recovery help e.g. OT, physio
Brown-Sequard Syndrome - aetiology, pathology, S&S, investigations
Condition a/w hemisection of the spinal cord, characterised by loss of temperature, pain, touch on one side (spinothalamic - sensory, contralateral) & paralysis on the other (corticospinal - motor, same side, iplatera)
`Causes; Spinal fractures, Gunshot wounds, Stab wounds, Crush injury, Inflammatory diseases, Tumours, Vertebral disc herniation, Vascular reasons include hemorrhage or ischemia.
Diagnostic imaging - MRI
EXAMPLE: R side of spine taken out - loss of sensory on L side & motor loss on R*
Describe a 3rd Nerve Palsy
Down & Out eye
fixed & dilated pupil
ptosis
Causes include: aneurysm of posterior communicating artery, infarction of nerve (diabetes), midbrain infarction or tumour
Define myotome & dermatome
Dermatome - area of skin supplied by single spinal nerve (sensory)
Myotome - group of muscles innervated by single spinal nerve (motor)
Myotome actions of Upper Limb
C4 - ‘‘shrug shoulders’’
C5 - shoulder ABduction, (elbows out & stop me from pushing them down), boxers pose (stop me from pulling them out)
C6 - shoulder aDDuction, (elbows out & stop me from pushing up), boxers pose (stop me from pulling them out), wrist flexion
C7 - elbow extension (boxers pose & push against me), wrist flexion
C8 - thumb ABduction (thumbs to sky & stop me from pushing them down)
T1 - finger ABduction (index finger, stop me pushing it in)
Myotomes of Lower Limb
L2 - hip flexion (raise leg up to sky) L5/S1 - hip extension (push down into bed)
L3 - knee extension (try & straighten leg) S1 - knee flexion
L4 - ankle dorsiflex (upwards)
L5 - big toe extension
S1 - ankle plantar flex (pedal)
Reflexes - Upper Limb
Triceps - C7
Biceps - C5/C6
Supinator - C5/C6
Reflexes - Lower Limb
Knee jerk - L3/L4 ‘‘kick the door’’
Ankle jerk - S1
Plantar - L5/S1
Meningitis - define, causes, S&S, ix & management
Definition: Inflammation of the meninges - outer membranes covering brain & spinal cord
Aetiology & Risk factors:
Can be due to number of infectious (viral vs bacterial) & non-infectious causes
Bacterial Meningitis
• Bacterial - Neisseria meningitidis (meningococcus, gram -ve diplococcus)
○ Meningococcal septicaemia - bacterial infection has entered bloodstream
§ Cause of classic non-blanching rash, indicated DIC & subcutaneous haemorrhages
○ Meningococcal meningitis - in the brain
• Bacterial - Streptococcus pneumoniae
• Bacterial (neonatal) - Group B Streptococcus
○ Usually contracted during birth from GBS vaginal bacteria
Viral Meningitis - tends to be milder & often only requires supportive treatment. Aciclovir can be used to treat suspected or confirmed HSV meningitis
• Herpes simplex virus (HSV)
• Enterovirus
• Varicella zoster virus (VZV
Presentation/Clinical Features: Signs & Symptoms • Fever • Neck stiffness • Vomiting • Headache • Photophobia • Altered consciousness • Seizures • Non-blanching rash (meningococcal septicaemia)
O/E - Kernig’s test & Brudzinski’s test
In Neonates
• Hypotonia
• Poor feeding
• Lethargy
• Bulging fontanelle
• Hypothermia
• LP should be performed in all children:
○ Under 1 months presenting with fever
○ 1 – 3 months with fever and are unwell
○ Under 1 years with unexplained fever and other features of serious illness
Investigations & Diagnosis:
Bedside/Community
• ABCDE - if critically unwell
• Focused history:
○ important to determine any preceding illnesses that increase risk of meningitis (e.g. sinusitis, otitis media, contact with an affected patient)
• Allergy status
• Formal examination
○ assess for meningeal irritation, look for non-blanching rash and signs of sepsis (e.g. hypotension, tachycardia)
• Throat Swab
• Respiratory viral screen (nasopharyngeal swab)
• STAT IM BENZYLPENICILLIN DOSE (1200 mg - adults, age adjusted for children)
Bloods • FBC, U&Es, LFTs, bone profile, coagulation, CRP • Blood cultures • Venous blood gas • Meningococcal PCR
Imaging
• CT head - usually done as part of work up, normally to r/o any contraindications for an LP
○ Some indications e.g. immunocompromised patient, hx of CNS disease, new onset seizures etc
Special Tests
• LUMBAR PUNCTURE (L3/L4)- every patient w/ suspected meningitis should undergo an LP & CSF evaulation
○ Ideally before abx, however difficult to implement in practise
○ Looks at: cell count & differential, protein, glucose, MC&S, viral PCR, save sample
○ May be able to isolate pathogen to tell if viral vs bacterial, but can also look at results of CSF
§ Bacterial = v high WCC, normal/reduced glucose & neutrophils
§ Viral = high WCC, normal glucose & lymphocytes
Management:
Depends on aetiology - usually treated for bacterial meningitis as really don’t want to miss it
Bacterial
• 1st line = ceftriaxone (3rd gen cephalosporin)
○ It should be used with caution in patients with penicillin allergy due to cross-reactivity
○ If there is a severe penicillin allergy (e.g. anaphylaxis) it should be avoided.
• 2nd line = chloramphenicol
Viral
• Majority secondary to enterovirus & don’t require any specific treatment
• Supportive measures inc rest, hydration, analgesia & anti-pyretic agent
• Aciclovir used if concern of encephalitis or HSV infection
Pathophysiology of movement disorder - MS, MG, MND
Multiple Sclerosis - autoimmune T cell mediated chronic demyelination in CNS, occurs sporadically throughout brain & spinal cord, lesions must be disseminated in time & space (UMN lesions)
Myaesthenia Gravis - autoimmune disorder characterised by muscle weakness & fatiguability, antibodies against AChR (LMN lesions)
Motor Neurone Disease or ALS - progressive selective loss/degeneration of neurones in the upper & lower motor tracts, sensory neurones are spared, eye movements never affected (LMN AND UMN)
Weber’s & Rinne’s Test Interpretation
WEBER’S
- normal = equal
- sensioneural loss = louder in ‘good ear’
- conductive loss = louder in bad ear
RINNE’S
- normal = AC > BC
- sensioneural = AC > BC due to both air and bone conduction being reduced equally
- conductive hearing loss = BC > AC
