Neuroscience Flashcards
Learning objectives
Answer
Define Bell’s palsy
• Idiopathic lower motor neurone facial nerve palsy
Explain the aetiology/risk factors of Bell’s palsy
- IDIOPATHIC
- 60% are preceded by an upper respiratory tract infection
- This suggests that it has a viral or post-viral aetiology
Summarise the epidemiology of Bell’s palsy
• Most cases: 20-50 yrs
Recognise the presenting symptoms of Bell’s palsy
• Prodrome of pre-auricular pain (in some cases)
• This is followed by unilateral facial weakness and droop
• Maximum severity: 1-2 days
• 50% experience facial, neck or ear pain or numbness
• Hyperacuisis
o This is due to stapedius paralysis
• Loss of taste (uncommon)
• Tearing or drying of exposed eye
o Because it may be difficult to close the eye fully
Recognise the signs of Bell’s palsy on physical examination
• Lower motor neurone weakness of facial muscles
o Affects ipsilateral muscles of facial expression
o Does NOT spare the muscles of the upper part of the face (unlike upper motor neurone facial nerve palsy)
• Bell’s Phenomenon
o Eyeball rolls up but the eye remains open when trying to close their eyes
• Despite reporting unilateral facial numbness, clinical testing of sensation is normal
• Examine the ears to check for other causes of facial nerve palsy (e.g. otitis media, herpes zoster infection)
Identify appropriate investigations for Bell’s palsy
- Usually unnecessary (except for excluding other causes)
* EMG - may show local axonal conduction block
Generate a management plan for Bell’s palsy
• Protection of cornea with protective glasses/patches or artificial tears
• High-dose corticosteroids is useful within 72 hrs
o Only given if Ramsey-Hunt Syndrome is excluded
• Surgery - lateral tarsorrhaphy (suturing the lateral parts of the eyelids together)
o Performed if imminent or established corneal damage
Identify possible complications of Bell’s palsy
• Corneal ulcers
• Eye infection
• Aberrant reinnervation
o E.g. Blinking may cause contraction of the angle of the mouth due to aberrant sympathetic innervation of orbicularis oculi and oris
o Crocodile Tears Syndrome - parasympathetic fibres may aberrantly reinnervate the lacrimal glands causing tearing whilst salivating
Summarise the prognosis for patients with Bell’s palsy
• 85-90% recover function within 2-12 weeks with or without treatment
Define central nervous system (CNS) tumours
- Tumours of the central nervous system.
- NOTE: brain tumours cannot be truly differentiated into benign and malignant because supposedly ‘benign’ tumours can cause significant morbidity and mortality
Instead they are differentiated into:
High-Grade = a tumour that grows rapidly and aggressively
• Glioma and glioblastoma multiforme
• Primary cerebral lymphoma
• Medulloblastoma
Low-Grade = a tumour that grows slowly and may or may not be successfully treated • Meningioma • Acoustic neuroma • Neurofibroma • Pituitary tumour • Craniopharyngeoma • Pineal tumour
Brain metastases commonly arise from: • Lung • Breast • Stomach • Prostate • Thyroid • Colorectal
Explain the aetiology / risk factors of central nervous system (CNS) tumours
• Can arise from any of the cells in the CNS (e.g. glial cells, ependymal cells, oligodendrocytes)
• Risk Factors
o Ionising radiation
o Immunosuppression (e.g. HIV)
o Inherited syndromes (e.g. neurofibromatosis, tuberous sclerosis)
Summarise the epidemiology of central nervous system (CNS) tumours
- Primary brain tumours = 2% of tumours diagnosed in the UK
- AIDS patients have an increased risk of developing CNS tumours
- Can develop at any age but are more common between 50-70 yrs
Recognise the presenting symptoms & signs of central nervous system (CNS) tumours
- Presentation depends on the size and location of the tumour
- Headache (worse in the morning and when lying down)
- Nausea and vomiting
- Seizures
- Progressive focal neurological deficits
- Cognitive and behavioural symptoms
- Papilloedema
Identify appropriate investigations for central nervous system (CNS) tumours and interpret the results
- Bloods - check CRP/ESR to eliminate other causes (e.g. temporal arteritis)
- CT/MRI
- Biopsy and tumour removal
- Magnetic resonance angiography - define changing size and blood supply of the tumour
- PET
- NOTE: distant metastases are RARE with primary CNS tumours
Define cluster headache
• A neurological disorder characterised by recurrent, severe headaches on one side of the head typically around the eye, tending to recur over a period of several weeks.
Explain the aetiology/risk factors of cluster headaches
- UNKNOWN aetiology
* Genetic factor implicated
Summarise the epidemiology of cluster headaches
- More common in MEN
* Usually occurs between 20-40 yrs
Recognise the presenting symptoms and signs of cluster headaches
• TWO types of cluster headaches:
o Episodic - occurring in periods lasting 7 days - 1 year, separated by pain-free periods lasting a month or longer. Cluster periods usually last between 2 weeks - 3 months
o Chronic - occurring for 1 year without remissions or with short-lived remissions of less than a month. Chronic cluster headaches can arise de novo or arise from episodic cluster headaches.
• Pattern of Occurrence
o Headaches occur in bouts lasting 6-12 weeks
o These occur once every year or once every 2 years, and tends to occur at the same time each year
o Headaches typically occurs at night, 1-2 hours after falling asleep
o The interval between bouts tends to be the same
o 10% with episodic cluster headaches go on to develop chronic cluster headaches
• Nature of Symptoms
o Pain comes on rapidly over around 10 mins
o Pain is intense, sharp and penetrating
o Pain is centred around the eye, temple or forehead
o Pain is unilateral
o Pain typically lasts around 45-90 mins (range: 15 mins - 3 hours)
o Pain occurs once or twice daily
o Associated autonomic features:
• Ipsilateral lacrimation
• Rhinorrhoea
• Nasal congestion
• Eye lid swelling
• Facial swelling
• Flushing
• Conjunctival injection
• Partial Horner’s syndrome
o Patients find it difficult to stay still and will pace around, occasionally banging their heads on things
• Triggers
o ALCOHOL - major precipitant
o Exercise and solvents
o Sleep disruption
Identify appropriate investigations for cluster headaches
- CLINICAL diagnosis based on history
* Neurological examination may be useful
Define encephalitis
• Inflammation of the brain parenchyma
Explain the aetiology / risk factors of encephalitis
Most commonly due to VIRAL INFECTION Viral Causes o Herpes Simplex Virus - MOST COMMON in the UK o VZV o Mumps o Adenovirus o Coxsackie o EBV o HIV o Japanese encephalitis Non-Viral (RARE) o Syphilis o Staphylococcus aureus In immunocompromised patients o CMV o Toxoplasmosis o Listeria Autoimmune or Paraneoplastic o Associated with certain antibodies (e.g. anti-NMDA, anti-VGKC)
Summarise the epidemiology of encephalitis
• UK incidence: 7.4/100,000
Recognise the presenting symptoms of encephalitis
- In most cases, encephalitis is self-limiting and mild
- Subacute onset (hours to days)
- Headache
- Fever
- Vomiting
- Neck stiffness
- Photophobia
- Behavioural changes
- Drowsiness
- Confusion
- History of seizures
- Focal neurological symptoms (e.g. dysphagia, hemiplegia)
- Obtain a detailed TRAVEL HISTORY
Recognise the signs of encephalitis on physical examination
- Reduce consciousness
- Deteriorating GCS
- Seizures
- Pyrexia
Signs of Meningism:
o Neck stiffness
o Photophobia
o Kernig’s test positive
Signs of raised ICP:
o Cushing’s Response: hypertension + bradycardia + irregular breathing
o Papilloedema
Focal neurological signs
MMSE may reveal cognitive/psychiatric disturbance
Identify appropriate investigations for encephalitis and interpret the results
Bloods o FBC - high lymphocytes (indicates viral cause) o U&Es - SIADH may occur as a result of encephalitis o Glucose o Viral serology o ABG MRI/CT o Exclude mass lesion o HSV causes oedema of the temporal lobe on MRI Lumbar Puncture o High lymphocytes o High monocytes o High protein o Glucose is usually normal o Viral PCR EEG - may show epileptiform activity Brain biopsy (rarely needed)
Define epilepsy
• A tendency to recurrent unprovoked seizures
• You need to have had > 2 seizures for epilepsy to be diagnosed
• Definition of Seizure: paroxysmal synchronised cortical electrical discharges
• Types of Seizure
o Focal Seizure: seizure localised to specific cortical regions (e.g. temporal lobe seizure). These can be further divided into:
• COMPLEX partial seizure: consciousness is affected
• SIMPLE partial seizure: consciousness is NOT affected
o Generalised Seizure: seizures that affect the whole of the brain. It also affects consciousness. There are different types of generalised seizure:
• Tonic-clonic
• Absence
• Myoclonic
• Atonic
• Tonic
Explain the aetiology/risk factors of epilepsy
• Most cases are IDIOPATHIC
• Primary epilepsy syndromes (e.g. idiopathic generalised epilepsy)
• Secondary Seizures
o Tumour
o Infection (e.g. meningitis)
o Inflammation (e.g. vasculitis)
o Toxic/Metabolic (e.g. sodium imbalance)
o Drugs (e.g. alcohol withdrawal)
o Vascular (e.g. haemorrhage)
o Congenital abnormalities (e.g. cortical dysplasia)
o Neurodegenerative disease (e.g. Alzheimer’s disease)
o Malignant hypertension or eclampsia
o Trauma
• Common things that look like seizures
o Syncope
o Migraine
o Non-epileptiform seizure disorder (e.g. dissociative disorder)
• Pathophysiology of Seizures
o Result from an imbalance in the inhibitory and excitatory currents or neurotransmission in the brain
o Precipitants include anything that promotes excitation of the cerebral cortex
o Often it is unclear why the precipitants cause seizures
Summarise the epidemiology of epilepsy
- COMMON
- 1% of the general population
- Typical age of onset: CHILDREN and ELDERLY
Recognise the presenting symptoms of epilepsy
• NOTE: try and obtain a collateral history from a witness as well as the patient
• Key features to consider when taking a history from a potential epilepsy patient:
o Rapidity of onset
o Duration of episode
o Any alteration in consciousness?
o Any tongue-biting or incontinence?
o Any rhythmic synchronous limb jerking?
o Any post-ictal abnormalities (e.g. exhaustion, confusion)?
o Drug history (alcohol, recreational drugs)
• Focal Seizure Presentation
o Frontal Lobe Focal Motor Seizure
• Motor convulsions
• May show a Jacksonian march (when the muscular spasm caused by the simple partial seizure spreads from affecting the distal part of the limb towards the ipsilateral face)
• May show post-ictal flaccid weakness (Todd’s paralysis)
o Temporal Lobe Seizures
• Aura (visceral or psychic symptoms)
• Hallucinations (usually olfactory or affecting taste)
o Frontal Lobe Complex Partial Seizure
• Loss of consciousness
• Involuntary actions/disinhibition
• Rapid recovery
• Generalised Seizures
o Tonic-Clonic (Grand Mal)
• Vague symptoms before attack (e.g. irritability)
• Tonic phase (generalised muscle spasm)
• Clonic phase (repetitive synchronous jerks)
• Faecal/urinary incontinence
• Tongue biting
• Post-ictal phase: impaired consciousness, lethargy, confusion, headache, back pain, stiffness
o Absence (Petit Mal)
• Onset in CHILDHOOD
• Loss of consciousness but MAINTAINTED POSTURE
• The patient will appear to stop talking and stare into space for a few seconds
• NO post-ictal phase
o Non-Convulsive Status Epilepticus
• Acute confusional state
• Often fluctuating
• Difficult to distinguish from dementia
Recognise the signs of epilepsy on physical examination
- Depends on aetiology
* Patients tend to be normal in between seizures
Identify appropriate investigations for epilepsy
• Bloods o FBC o U&E o LFTs o Glucose o Calcium o Magnesium o ABG o Toxicology screen o Prolactin - shows a transient increase shortly after seizures • EEG o Helps to confirm diagnosis o Helps classify the epilepsy o Ictal EEGs are particularly useful (i.e. during a seizure) • CT/MRI o Shows structural, space-occupying or vascular lesions • Other investigations o If it is suspected to be a secondary seizure (e.g. due to infection)
Generate a management plan for epilepsy
• Treatment of STATUS EPILEPTICUS
o DEFINITION of Status Epilepticus: a seizure lasting > 30 mins or repeated seizure without recovery and regain of consciousness in between
o Although the definition states that the seizure must last > 30 mins, treatment is usually initiated early (after around 5-10 mins)
o ABC approach
o Check GLUCOSE (give glucose if hypoglycaemic)
o IV lorazepam OR IV/PR diazepam - REPEAT again after 10 mins if seizure does not terminate
o If seizures recur following the next dose of lorazepam or diazepam, consider IV phenytoin - an ECG monitor is required
• NOTE: other agents include phenobarbitone, levetiracetam and sodium valproate
o If this also fails, consider general anaesthesia (e.g. thiopentone) - intubation and mechanical ventilation required
o Treat the CAUSE (e.g. hypoglycaemia or hyponatraemia)
o Check plasma levels of anticonvulsants (because status epilepticus is often caused by lack of compliance with anti-epileptic medications)
• Treatment of newly diagnosed epilepsy
o Only start anti-convulsant treatment after > 2 unprovoked seizures
o FOCAL Seizure 1st Line: lamotrigine or carbamazepine
o GENERALISED Seizure 1st Line: sodium valproate
o Start treatment with only ONE anti-epileptic drug
o Other anti-convulsants: phenytoin, levetiracetam, clobazam, topiramate, gabapentin, vigabatrin
• Patient Education
o Avoid triggers
o Use seizure diaries
o Particular consideration for women of child-bearing age because the anti-epileptic drugs can have teratogenic effects
o Be careful of drug interactions (e.g. AEDs can reduce the effectiveness of the oral contraceptive pill)
• Surgery may be considered for refractory epilepsy
Identify possible complications of epilepsy
• Fractures from tonic-clonic seizures • Behavioural problems • Sudden death in epilepsy (SUDEP) • Complications of anti-epileptic drugs: o Gingival hypertrophy (phenytoin) o Neutropaenia and osteoporosis (carbamazepine) o Stevens-Johnson syndrome (lamotrigine)
Summarise the prognosis for patients with epilepsy
• 50% remission at 1 year
Define extradural haemorrhage
• Bleeding and accumulation of blood in the extradural space
Explain the aetiology / risk factors of extradural haemorrhage
TRAUMA
o Usually due to fracture of the temporal or parietal bones leading to rupture of the middle meningeal artery
Risk Factors
o Bleeding tendency
• E.g. haemophilia, anticoagulant therapy
Summarise the epidemiology of extradural haemorrhage
- UK incidence: 20/10,000
- 10% of severe head injuries
- Most commonly seen in YOUNG ADULTS
Recognise the signs of extradural haemorrhage on physical examination
- Head injury with temporary loss of consciousness
- Followed by lucid interval
- Followed by progressive deterioration in conscious level
Recognise the presenting symptoms of extradural haemorrhage
• Scalp trauma or fracture • Headache • Deteriorating GCS Signs of raised ICP o E.g. dilated, unresponsive pupil on the side of the injury Cushing's Reflex o Hypertension o Bradycardia o Irregular breathing
Identify appropriate investigations for extradural haemorrhage and interpret the results
• Urgent CT Scan
o Check for a haematoma
o Look for features of raised ICP (e.g. midline shift)
Define Guillain-Barre syndrome
• Acute inflammatory demyelinating polyneuropathy
Explain the aetiology/risk factors of Guillain-Barre syndrome
• An inflammatory process where antibodies after a recent infection react with self-antigen on myelin or neurons
• There is often no aetiological trigger identified (40% of cases are idiopathic)
• Other causes:
o Post-infection (1-3 weeks) - bacterial, HIV, herpes viruses
o Malignancy - e.g. lymphoma
o Post-vaccination
Summarise the epidemiology of Guillain-Barre syndrome
- UK incidence: 1-2/100,000
* Affects all age groups
Recognise the presenting symptoms of Guillain-Barre syndrome
• PROGRESSIVE symptoms
• < 1 month duration of:
o ASCENDING symmetrical limb weakness (lower > upper)
o ASCENDING paraesthesia
• Cranial nerve involvement (leading to, for example, dysphagia, dysarthria, facial weakness)
• Respiratory muscles may be affected in SEVERE cases
• Miller-Fisher Variant (RARE) = ophthalmoplegia, ataxia, arreflexia
Recognise the signs of Guillain-Barre syndrome on physical examination
• General MOTOR Examination
o Hypotonia
o Flaccid paralysis
o Arreflexia (ascending upwards from feet to head)
• General SENSORY Examination
o Impairment of sensation in multiple modalities (ascending from feet to head)
• Cranial Nerve Palsies
o Facial nerve weakness
o Abnormality of external ocular movements
o If pupil constriction is affected, consider botulism
• Type II Respiratory Failure
o Due to paralysis of respiratory muscles
• Autonomic Function
o Assess postural blood pressure change and arrhythmias
Identify appropriate investigations for Guillain-Barre syndrome
• Lumbar Puncture o HIGH protein o NORMAL cell count and glucose • Nerve Conduction Study o Reduced conduction velocity o NOTE: it may be normal in the early stages of the disease • Bloods o Anti-ganglioside antibodies in Miller-Fisher variant + 25% of Guillain-Barre cases • Spirometry o Reduced fixed vital capacity - suggests ventilatory weakness • ECG o Arrhythmias may develop
Define Horner’s Syndrome
• A condition that results from the disruption of the sympathetic nerves supplying the face resulting in a triad of: o Ptosis o Miosis o Anhydrosis o (and enophthalmos)
Explain the aetiology/risk factors of Horner’s syndrome
• It is caused by disruption of the sympathetic nerves • Causes o Strokes o Multiple sclerosis o Apical lung tumours o Lymphadenopathy o Basal skull tumours o Carotid artery dissection o Neck trauma
Summarise the epidemiology of Horner’s syndrome
- RARE
* Important sign that is associated with various diseases (most notably, Pancoast tumours)
Recognise the presenting symptoms of Horner’s syndrome
- Inability to open the eye fully on the affected side
- Loss of sweating on affected side
- Facial flushing
- Orbital pain/headache
- Other symptoms based on CAUSE
Recognise the signs of Horner’s syndrome on physical examination
- Ptosis
- Miosis
- Anhydrosis
- Enophthalmos
Identify appropriate investigations for Horner’s syndrome
- Investigations are directed towards figuring out the underlying cause
- CXR - apical lung tumour
- CT/MRI - cerebrovascular accidents
- CT angiography - dissection
Generate a management plan for Horner’s syndrome
- Horner’s syndrome is a sign not a disease in itself
- So, the management depends on the cause (e.g. management for carotid dissection is very different to management of apical lung tumours)
Identify possible complications of Horner’s syndrome
• Depends on cause
Summarise the prognosis of Horner’s syndrome
• Depends on the cause
Define Huntington’s disease
• Autosomal dominant trinucleotide repeat disease characterised by progressive chorea and dementia, typically commencing in middle age
Explain the aetiology/risk factors of Huntington’s disease
- The huntingtin gene codes for a protein called huntingtin
- In the huntingtin gene there is a trinucleotide repeat expansion (CAG) that results in toxic gain of function
- Autosomal DOMINANT
- Earlier age of onset with each successive generation
Summarise the epidemiology of Huntington’s disease
• Average age of onset: 30-50 yrs
Recognise the presenting symptoms of Huntington’s disease
• Family history • INSIDIOUS onset in middle-age • Progressive • Fidgeting • Clumsiness • Involuntary, jerky, dyskinetic movements often accompanied by grunting and dysarthria • EARLY COGNITIVE CHANGES: o Lability o Dysphoria (a state of unease or generalised dissatisfaction with life) o Mental inflexibility o Anxiety o Develops into dementia • LATER STAGES: o Rigid o Akinetic o Bed-bound • Enquire about drug history (especially cocaine and anti-psychotics)
Recognise the signs of Huntington’s disease on physical examination
- Chorea
- Dysarthria
- Slow voluntary saccades
- Supranuclear gaze restriction
- Parkinsonism
- Dystonia
- MMSE shows cognitive and emotional deficits
Identify appropriate investigations for Huntington’s disease
• Genetic Analysis
o Diagnostic if there are > 39 CAG repeats in the HD gene
o Reduced penetrance leads to an intermediate number of CAG repeats
• Imaging
o Brain MRI or CT may show symmetrical atrophy of the striatum and butterfly dilation of the lateral ventricles
• Bloods
o To exclude other pathology
Define hydrocephalus
• Enlargement of the cerebral ventricular system.
• It can be subdivided into obstructive and non-obstructive
o AKA communicating and non-communicating
• Hydrocephalus ex vacuo = apparent enlargement of the ventricles as a compensatory change due to brain atrophy
Explain the aetiology/risk factors of hydrocephalus
• Abnormal accumulation of CSF in the ventricles can be caused by:
o OBSTRUCTIVE: Impaired outflow of the CSF from the ventricular system
• Lesions of the 3rd and 4th ventricle or cerebral aqueduct
• Posterior fossa lesions (e.g. tumour) compressing the 4th ventricle
• Cerebral aqueduct stenosis
o NON-OBSTRUCTIVE: Impaired CSF reabsorption into the subarachnoid villi
• Tumours
• Meningitis
• Normal Pressure Hydrocephalus - idiopathic chronic ventricular enlargement. The long white matter tracts are damaged leading to gait and cognitive decline
Summarise the epidemiology of hydrocephalus
• Bimodal age distribution
o YOUNG - congenital malformations and brain tumours
o ELDERLY - strokes and tumours
Recognise the presenting symptoms of hydrocephalus
• Obstructive Hydrocephalus o Acute drop in conscious level o Diplopia • Normal Pressure Hydrocephalus o Triad of symptoms: • Dementia • Gait disturbance • Urinary incontinence
Recognise the signs of hydrocephalus on physical examination
• Obstructive Hydrocephalus o Low GCS o Papilloedema o 6th nerve palsy • 6th nerve has the longest intracranial path of all the cranial nerves and so is most susceptible to palsy due to raised ICP o NEONATES:
• Increased head circumference • Sunset sign (downward conjugate deviation of the eyes) • Normal Pressure Hydrocephalus o Cognitive impairment o Gait apraxia (shuffling) o Hyperreflexia
Identify appropriate investigations for hydrocephalus
• CT Head
o FIRST-LINE for detecting hydrocephalus
o May also pick up the cause (e.g. tumour)
• CSF
o From ventricular drain or lumbar puncture
o May indicate pathology (e.g. tuberculosis)
o Check MC&S, protein and glucose
• Lumbar Puncture
o IMPORTANT: contraindicated if raised ICP
o Therapeutic in normal pressure hydrocephalus
Define meningitis
• Inflammation of the leptomeningeal (pia and arachnoid mater) coverings of the brain, most commonly due to infection
Explain the aetiology / risk factors of meningitis
BACTERIAL Neonates • Group B streptococci • Escherichia coli • Listeria monocytogenes Children • Haemophilus influenzae • Neisseria meningitidis • Streptococcus pneumoniae Adults • Neisseria meningitidis • Streptococcus pneumoniae • Tuberculosis Elderly • Streptococcus pneumoniae • Listeria monocytogenes
VIRAL o Enteroviruses o Mumps o HSV o VZV o HIV
Fungal o Cryptococcus (common cause of meningitis in HIV patients)
Others
o Aseptic meningitis (not due to microbes)
o Mollaret’s meningitis (recurrent benign lymphocytic meningitis)
RISK FACTORS o Close communities (e.g. college halls) o Basal skull fractures o Mastoiditis o Sinusitis o Inner ear infections o Alcoholism o Immunodeficiency o Splenectomy o Sickle cell anaemia o CSF shunts o Intracranial surgery
Summarise the epidemiology of meningitis
• UK: 2500 notifications/yr
Recognise the presenting symptoms of meningitis
- Severe headache
- Photophobia
- Neck or backache
- Irritability
- Drowsiness
- Vomiting
- High-pitched crying or fits (common in children)
- Reduced consciousness
- Fever
IMPORTANT: take a good travel history and exposure history and take not of exposure to any of the following
o Rodents (lymphocytic choriomeningitis virus)
o Ticks (Lyme borrelia, Rocky Mountain spotted fever)
o Mosquitoes (West Nile virus)
o Sexual activity (HSV-2, HIV, syphilis)
o Travel
Recognise the signs of meningitis on physical examination
• Signs of MENINGISM
o Photophobia
o Neck stiffness
o Kernig’s Sign - with the hips flexed, there is pain/resistance on passive knee extension
o Brudzinski’s Sign - flexion of the hips when the neck is flexed
• Signs of INFECTION o Fever o Tachycardia o Hypotension o Skin rash o Altered mental state
Identify appropriate investigations for meningitis and interpret the results
Bloods
o Two sets of blood cultures
Imaging
o CT scan - exclude mass lesion or raised ICP before LP
Lumbar Puncture o MC&S o Bacterial meningitis: • Cloudy CSF • High neutrophils • High protein • Low glucose o Viral meningitis: • High lymphocytes • High protein • Normal glucose o TB meningitis: • Fibrinous CSF • High lymphocytes • High protein • Low glucose
Generate a management plan for meningitis
IMMEDIATE IV Antibiotics (before LP)
o First choice: 3rd generation cephalosporin (e.g. cefotaxime or ceftriaxone)
o Benzylpenicillin may be used as an initial blind therapy
Dexamethasone IV
o Given shortly before or with the first dose of antibiotics
o Associated with a reduced risk of complications
Resuscitation
o Manage in ITU
o Notify public health services
Identify the possible complications of meningitis and its management
- Septicaemia
- Shock
- DIC
- Renal failure
- Seizures
- Peripheral gangrene
- Cerebral oedema
- Cranial nerve lesions
- Cerebral venous thrombosis
- Hydrocephalus
- Waterhouse-Friderichsen Syndrome (bilateral adrenal haemorrhage caused by severe meningococcal infection)
Summarise the prognosis for patients with meningitis
- Mortality rate from bacterial meningitis: 10-40% with meningococcal sepsis
- Viral meningitis is self-limiting
Define migraine
• Severe episodic headache that may have a prodrome of focal neurological symptoms (aura) and is associated with systemic disturbance.
• Can be classified as:
o Migraine with aura (classical migraine)
o Migraine without aura (common migraine)
o Migraine variants (e.g. familial hemiplegic, ophthalmoplegic)
Explain the aetiology/risk factors of migraine
- Poorly understood
- Early aura of cortical spreading depression is associated with intracranial vasoconstriction leading to localised ischaemia
- This is then followed by meningeal and extracranial vasodilation mediated by serotonin, bradykinin and the trigeminovascular system
Summarise the epidemiology of migraine
• Prevalence:
o Males - 6%
o Females - 15-20%
• Usually occurs in adolescence and early adulthood
Recognise the presenting symptoms of migraine
• Headache o Pulsatile o Duration 4-72 hrs o Episodic o NOTE: chronic daily headaches lasting weeks would suggest a different aetiology • Associated Symptoms o Nausea o Vomiting o Photophobia/Phonophobia o Aura: • Flashing lights • Spots • Blurring • Zigzag lines • Blind spots (scotomas) • Tingling/numbness in the limbs • Triggers and Risk Factors o Stress o Exercise o Lack of sleep o Oral contraceptive pill o Foods (e.g. caffeine, alcohol, cheese, chocolate)
Recognise the signs of migraine on physical examination
- NO specific physical findings
* Exclude secondary causes with MMSE, neurological examination, fundoscopy etc.
Identify appropriate investigations for migraine
- Diagnosis is usually based on HISTORY
- Investigations may be useful for excluding other diagnoses
- Bloods, CT/MRI, lumbar puncture
Generate a management plan for migraine
• NOTE: analgesia overuse can cause headaches • ACUTE o NSAIDs o Paracetamol o Codeine o Antiemetics o Triptans (5-HT agonists) - e.g. sumatriptan • Prophylaxis o -blockers o Amitriptyline o Topiramate o Sodium valproate o Menstrual migraines can be controlled with the oral contraceptive pill • Advice o Avoid triggers o Rest in a quiet dark room during episodes
Identify possible complications of migraine
- Disruption of daily activities
* Can lead to analgesia-overuse headaches in people who use analgesia regularly
Summarise the prognosis for patients with migraine
- Usually CHRONIC
* Most cases can be managed well with preventative/early treatment measures
Define motor neurone disease
• A progressive neurodegenerative disorder of cortical, brainstem and spinal motor neurons (lower and upper motor neurons) • Subtypes: o Amyotrophic Lateral Sclerosis (ALS) • AKA Lou Gehrig's disease • Combined generation of upper AND lower motor neurones resulting a mix of LMN and UMN signs o Progressive Muscular Atrophy Variant • Only LMN signs • Better prognosis o Progressive Bulbar Palsy Variant • Dysarthria • Dysphagia • Wasted fasciculating tongue • Brisk jaw jerk reflex o Primary Lateral Sclerosis Variant • UMN pattern of weakness • Brisk reflexes • Extensor plantar responses • NO LMN signs
Explain the aetiology/risk factors of motor neurone disease
• UNKNOWN
• Free radical damage and glutamate excitotoxicity have been implicated
• Pathology
o Progressive motor neurone degeneration and death
o Gliosis replacing lost neurones
• Associations
o Frontotemporal lobar dementia
Summarise the epidemiology of motor neurone disease
- RARE
- Incidence: 2/100,000
- Mean age of onset: 55 yrs
- 5-10% have a family history with autosomal dominant inheritance
Recognise the presenting symptoms of motor neurone disease
- Weakness of limbs
- Speech disturbance (slurring or reduction in volume)
- Swallowing disturbance (e.g. choking on food)
- Behavioural changes (e.g. disinhibition, emotional lability)
Recognise the signs of motor neurone disease on physical examination
• Combination of UMN and LMN signs • LMN Features o Muscle wasting o Fasciculations o Flaccid weakness o Hyporeflexia • UMN Features o Spastic weakness o Extensor plantar response o Hyperreflexia • Sensory examination - should be NORMAL
Identify appropriate investigations for motor neurone disease
• Bloods
o Mild elevation in CK
o ESR
o Anti-GM1 ganglioside antibodies
• Electromyography (EMG)
• Nerve conduction studies - often normal
• MRI - exclude cord compression and brainstem lesions
• Spirometry - assess respiratory muscle weakness
Define multiple sclerosis
• Inflammatory demyelinating disease of the CNS
• Types
o Relapsing-Remitting MS
• COMMONEST form
• Clinical attacks of demyelination with complete recovery in between attacks
o Clinically Isolated Syndrome
• Single clinical attack of demyelination
• The attack in itself does NOT count as MS
• 10-50% progress to develop MS
o Primary Progressive MS
• Steady accumulation of disability with NO relapsing-remitting pattern
o Marburg Variant
• Severe fulminant variant of MS leading to advanced disability or death within weeks
Explain the aetiology/risk factors of multiple sclerosis
• UNKNOWN
• Autoimmune basis with potential environmental trigger in genetically susceptible individuals
• Immune-mediated damage to myelin sheaths results in impaired axonal conduction
• Risk Factors
o EBV exposure
o Prenatal vitamin D levels
Summarise the epidemiology of multiple sclerosis
- UK prevalence: 1/1000
- 2 x as common in FEMALES
- Age of presentation: 20-40 yrs
Recognise the presenting symptoms of multiple sclerosis
• Varies depending on the site of inflammation • Optic Neuritis (COMMONEST) o Unilateral deterioration of visual acuity and colour perception o Pain on eye movement o Common first symptoms of multiple sclerosis • Sensory o Pins and needles o Numbness o Burning • Motor o Limb weakness o Spasms o Stiffness o Heaviness • Autonomic o Urinary urgency o Hesitancy o Incontinence o Impotence • Psychological o Depression o Psychosis • Uhthoff's Sign - worsening of neurological symptoms as the body gets overheated from hot weather, exercise, saunas, hot tubs etc. • Lhermitte's Sign - an electrical sensation that runs down the back and into the limbs when the neck is flexed
Recognise the signs of multiple sclerosis on physical examination
• Optic Neuritis
o Impaired visual acuity (MOST COMMON)
o Loss of coloured vision
• Visual Field Testing
o Central scotoma (if optic nerve is affected)
• Scotoma = a blind spot in the normal visual field
o Field defects (if optic radiations are affected)
• Relative Afferent Pupillary Defect (RAPD)
• Internuclear Ophthalmoplegia
o Lateral horizontal gaze causes failure of adduction of the contralateral eye
o Indicates lesion of the contralateral medial longitudinal fasciculus
• Sensory
o Paraesthesia
• Motor
o UMN signs
• Cerebellar
o Limb ataxia (intention tremor, past-pointing, dysmetria)
o Dysdiadochokinesia
o Ataxic wide-based gait
o Scanning speech
Identify appropriate investigations for multiple sclerosis
• Diagnosis is based on the finding of two or more CNS lesions with corresponding symptoms, separated in time and space - McDONALD CRITERIA
• Lumbar Puncture
o Microscopy - exclude infection/inflammatory causes
o CSF electrophoresis shows unmatched oligoclonal bands
• MRI Brain, Cervical and Thoracic Spine (with gadolinium)
o Plaques can be identified
o Gadolinium enhancement shows active lesions
• Evoked Potentials
o Visual, auditory and somatosensory evoked potentials may show delayed conduction velocity
Define myasthenia gravis
• An autoimmune disease affecting the neuromuscular junction producing weakness in skeletal muscles
Explain the aetiology/risk factors of myasthenia gravis
- Impairment of neuromuscular junction transmission
- Most commonly due to autoantibodies against the nicotinic acetylcholine receptor
- Lambert-Eaton Syndrome - paraneoplastic subtype of myasthenia gravis caused by autoantibodies against pre-synaptic calcium channels, leading to impairment of acetylcholine release
- Myasthenia gravis is associated with other autoimmune conditions (e.g. pernicious anaemia)
Summarise the epidemiology of myasthenia gravis
- Prevalence: 8-9/100,000
- More common in FEMALES at younger ages
- Equal gender distribution in middle age
Recognise the presenting symptoms of myasthenia gravis
• Muscle weakness that worsens with repetitive use or towards the end of the day
o NOTE: in Lambert-Eaton syndrome, muscle weakness improves after repeated use
• Ocular symptoms
o Drooping eyelids
o Diplopia
• Bulbar symptoms
o Facial weakness (myasthenic snarl)
o Disturbed hypernasal speech
o Difficulty smiling, chewing or swallowing
Recognise the signs of myasthenia gravis on physical examination
• May be generalised (affecting many muscle groups)
• May be bulbar (affecting the bulbar muscles i.e. those associated with cranial nerves 9, 10, 11 and 12)
o NOTE: bulbar = relating to the medulla oblongata (cranial nerves 9, 10, 11 and 12 have their nuclei in the medulla)
• May be ocular
• Eye Signs
o Ptosis
o Complex ophthalmoplegia
o Check for ocular fatigue by asking the patient to sustain and upward gaze for 1 min and watch the progressive ptosis that develops
• Ice on Eyes Test
o Placing ice packs on closed eyelids for 2 mins can improve neuromuscular transmission and reduce ptosis
• Bulbar Signs
o Reading aloud may cause dysarthria or nasal speech
• Limbs
o Test the power of a muscle before and after repeated use of the muscle
Identify appropriate investigations for myasthenia gravis
• Bloods
o CK - exclude myopathies
o Serum acetylcholine receptor antibody (positive in 80%)
o TFTs (it is associated with hyperthyroidism)
o Anti-voltage gated calcium channel antibody (in Lambert-Eaton syndrome)
• Tensilon Test
o Short-acting anti-cholinesterase (edrophonium bromide) increases acetylcholine levels and causes a rapid and transient improvement in clinical features
o Risk of bradycardia - so is generally avoided
• Nerve Conduction Study
o Repetitive stimulation shows decrements of muscle action potential
• EMG
• CT Thorax/CXR - visualise thymoma in the mediastinum or lung malignancies
Define neurofibromatosis
• An autosomal dominant genetic disorder affecting cells of neural crest origin, resulting in the development of multiple neurocutaneous tumours • Type 1 Neurofibromatosis (von Recklinghausen's disease) o Characterised by: • Peripheral and spinal neurofibromas • Multiple café au lait spots • Freckling (axillary/inguinal) • Optic nerve glioma • Lisch nodules (on iris) • Skeletal deformities • Phaeochromocytomas • Renal artery stenosis • Type 2 Neurofibromatosis o Characterised by: • Schwannomas (often bilateral vestibular schwannomas) • Meningiomas • Gliomas • Cataracts
Explain the aetiology/risk factors of neurofibromatosis
• Associated with multiple mutations in tumour suppressor genes NF1 (type 1) and NF2 (type 2)
Summarise the epidemiology of neurofibromatosis
• No gender or racial predilection
Recognise the presenting symptoms of neurofibromatosis
• Positive family history (however, 50% are caused by new mutations) • Type 1 o Skin lesions o Learning difficulties (40%) o Headaches o Disturbed vision (due to optic gliomas) o Precocious puberty (due to lesions of the pituitary gland from an optic glioma involving the chiasm) • Type 2 o Hearing loss o Tinnitus o Balance problems o Headache o Facial pain o Facial numbness
Recognise the signs of neurofibromatosis on physical examination
• Type 1
o 5+ café au lait macules of > 5 mm (prepubertal)
o 5+ café au lait macules of > 15 mm (post-pubertal)
o Neurofibromas (may appear as cutaneous nodules or complex plexiform neuromas)
o Freckling in armpit or groin
o Lisch nodules (hamartomas on the iris)
o Spinal scoliosis
• Type 2
o Few or no skin lesions
o Sensorineural deafness with facial nerve palsy or cerebellar signs (if the schwannoma is large)
Identify appropriate investigations for neurofibromatosis
- Ophthalmological assessment
- Audiometry
- MRI brain and spinal cord - for vestibular schwannomas, meningiomas and nerve root neurofibromas
- Skull X-ray (sphenoid dysplasia in NF1)
- Genetic testing
Define Parkinson’s disease
• Neurodegenerative disease of the dopaminergic neurones of the substantia nigra, characterised by:
o Bradykinesia
o Rigidity
o Resting tremor
o Postural instability
• Pathophysiology
o Degeneration of dopaminergic neurones projecting from the substantia nigra to the striatum
o Patients are only symptomatic after the loss of > 70% of dopaminergic neurones
Explain the aetiology/risk factors of Parkinson’s disease
• Sporadic/Idiopathic Parkinson’s Disease
o Most COMMON
o Aetiology UNKNOWN
o May be related to environmental toxins and oxidative stress
• Secondary Parkinson’s Disease
o Neuroleptic therapy (e.g. for schizophrenia)
o Vascular insults (e.g. in the basal ganglia)
o MPTP toxin from illicit drug contamination
o Post-encephalitis
o Repeated head injury
• There are some familial forms of Parkinson’s disease
Summarise the epidemiology of Parkinson’s disease
- Very COMMON
- Prevalence: 1-2% of > 60 yrs
- Mean age of onset: 57 yrs
Recognise the presenting symptoms of Parkinson’s disease
- INSIDIOUS onset
- Resting tremor (mainly in hands)
- Stiffness and slowness of movements
- Difficulty initiating movements
- Frequent falls
- Smaller hand writing (micrographia)
- Insomnia
- Mental slowness (bradyphenia)
Recognise the signs of Parkinson’s disease on physical examination
• Tremor o Pill rolling rest tremor o 4-6 Hz o Decreased on action o Usually asymmetrical • Rigidity o Lead pipe rigidity of muscle tone o Superimposed tremor can cause cogwheel rigidity o Rigidity can be enhanced by distraction • Gait o Stooped o Shuffling o Small-stepped gait o Reduced arm swing o Difficulty initiating walking • Postural Instability o Falls easily with little pressure from the back or the front • Other features o Frontalis overactivation (leads to furrowing of the brow) o Hypomimic face o Soft monotonous voice o Impaired olfaction o Tendency to drool o Mild impairment of up-gaze • Psychiatric o Depression o Cognitive problems and dementia (in later stages)
Identify appropriate investigations for Parkinson’s disease
• CLINICAL diagnosis
• Levodopa Trial
o Timed walking and clinical assessment after administration of levodopa
• Bloods
o Serum caeruloplasmin - rule out Wilson’s disease as a cause of Parkinson’s disease
• CT or MRI Brain
o To exclude other causes of gait decline (e.g. hydrocephalus)
• Dopamine Transporter Scintigraphy
o Reduction in striatum and putamen
Define spinal cord compression
• Injury to the spinal cord with neurological symptoms dependent on the site and extent of the injury
Explain the aetiology/risk factors of spinal cord compression
• MOST CASES: trauma and tumours • Trauma can lead to compression by: o Direct cord contusion o Compression by bone fragments o Haematoma o Acute disk prolapse • Tumours are more frequently METASTASES • Other causes: spinal abscess, TB (Pott's disease) • Risk Factors o Trauma o Osteoporosis o Metabolic bone disease o Vertebral disc disease
Summarise the epidemiology of cord compression
- COMMON
- Trauma occurs across all age groups
- Malignancy/disc disease is more common in the ELDERLY
Recognise the presenting symptoms of cord compression
• History of trauma or malignancy
• Pain
• Weakness
• Sensory loss
• Disturbance of bowel and bladder function
• A large central lumbar disc prolapse may cause:
o Bilateral sciatica
o Saddle anaesthesia (loss of sensation in the area of the buttocks that is covered by a bike seat)
o Urinary retention
Recognise the signs of cord compression on physical examination
• Diaphragmatic breathing
• Reduced anal tone
• HYPOreflexia
• Priapism (persistent and painful erection)
• Spinal shock (low blood pressure without tachycardia)
• Sensory Loss - at level of the lesion
• Motor
o Weakness or paralysis
o Downward plantars (in acute phase)
o UMN signs below the level of the lesion
o LMN signs at the level of the lesion
• Brown-Sequard Syndrome - seen with hemisection of the spinal cord
Identify appropriate investigations for cord compression
• Radiology
o Lateral radiographs of spine to look for loss of alignment, fractures etc.
o MRI or CT
• Bloods - FBC, U&Es, calcium, ESR, immunoglobulin electrophoresis (multiple myeloma)
• Urine - look for Bence Jones proteins (multiple myeloma)
Define sciatica
• Pain, tingling and numbness that arise from nerve root compression or irritation in the lumbosacral spine.
Explain the aetiology/risk factors of sciatica
• Most commonly caused by a disc herniation
• Other causes:
o Spinal stenosis
o Spondylolisthesis
o Spinal injury or infection
o Tumour
o Cauda equina syndrome
• Risk Factors
o Age - older people are more like to get slipped discs
o Job that requires regular heavy lifting
Summarise the epidemiology of sciatica
- Relatively COMMON
* More common in MALES
Recognise the presenting symptoms and signs of sciatica
- Pain (usually affects the buttocks and the legs more than the back)
- Numbness
- Tingling sensation that radiates from the lower back down one of the legs
- Weakness in the calf muscles or the muscles that move the foot or ankle
Identify appropriate investigations for sciatica
- CLINICAL diagnosis
- Straight Leg Raise
o If pain in the distribution of the sciatic nerve is reproduced on passive flexion of the straight leg at the hip between 30-70 degrees then it is considered a positive sign (Lasegue’s sign)
o This test is sensitive but not very specific
• CT/MRI - helps visualise a lumbar disc herniation
Define stroke (ischaemic and haemorrhagic)
• Rapid permanent neurological deficit from cerebrovascular insult. Also defined clinically, as focal or global impairment of CNS function developing rapidly and lasting > 24 hrs
• Can be subdivided based on:
o Location - anterior circulation vs posterior circulation
o Pathological Process - infarction vs haemorrhage
Explain the aetiology / risk factors of stroke (ischaemic and haemorrhagic)
INFARCTION (80%)
Thrombosis
• Can occur in small vessels (lacunar infarcts)
• Can occur in larger vessels (e.g. middle cerebral artery)
• Can arise in prothrombotic states (e.g. dehydration, thrombophilia)
Emboli
• From carotid dissection, carotid atherosclerosis, atrial fibrillation
• NOTE: they can arise from venous blood clots that pass through a septal defect (e.g. VSD) and get lodged in the cerebral circulation
Hypotension
• If the blood pressure is below the autoregulatory range required to maintain cerebral blood flow, you can get infarction in the watershed zones between different cerebral artery territories
Others
• Vasculitis
• Cocaine (arterial spasm)
HAEMORRHAGE (10%)
o Hypertension
o Charcot-Bouchard microaneurysm rupture (DEFINITION: aneurysms within the brain vasculature that occur in small blood vessels)
o Amyloid angiopathy
o Arteriovenous malformations
o Less common: trauma, tumours, vasculitis
Summarise the epidemiology of stroke (ischaemic and haemorrhagic)
- COMMON
- Incidence: 2/1000
- 3rd most common cause of death in industrialised countries
- Usual age of stroke patients: 70+
Recognise the presenting symptoms of stroke (ischaemic and haemorrhagic)
- SUDDEN-ONSET
- Weakness
- Sensory, visual or cognitive impairment
- Impaired coordination
- Impaired consciousness
- Head or neck pain (if carotid or vertebral artery dissection)
- Enquire about time of onset (critical for emergency management if < 4.5 hrs)
- Enquire about history of AF, MI, valvular heart disease, carotid artery stenosis, recent neck trauma or pain
Recognise the signs of stroke (ischaemic and haemorrhagic) on physical examination
- Examine for underlying cause (e.g. atrial fibrillation)
- Infarction
Lacunar Infarcts
• Affecting the internal capsule or pons: pure sensory or motor deficit (or both)
• Affecting the thalamus: loss of consciousness, hemisensory deficit
• Affecting the basal ganglia: hemichorea, hemiballismus, parkinsonism
Anterior Circulation
• Anterior Cerebral
Lower limb weakness
Confusion
Middle Cerebral Facial weakness Hemiparesis (motor cortex) Hemisensory loss (sensory cortex) Apraxia Hemineglect (parietal lobe) Receptive or expressive dysphasia (due to involvement of Wernicke's and Broca's areas) Quadrantopia (if superior or inferior optic radiations are affected)
Posterior Circulation
• Posterior Cerebral - hemianopia
• Anterior Inferior Cerebellar - vertigo, ipsilateral ataxia, ipsilateral deafness, ipsilateral facial weakness
• Posterior Inferior Cerebellar (affected in lateral medullary syndrome) - vertigo, ipsilateral ataxia, ipsilateral Horner’s syndrome, ipsilateral hemisensory loss, dysarthria, contralateral spinothalamic sensory loss
• Basilar Artery - cranial nerve pathology and impaired consciousness
• Multiple Lacunar Infarcts - vascular dementia, urinary incontinence, gait apraxia, shuffling gait, normal or excessive arm-swing
• Intracerebral - headache, meningism, focal neurological signs, nausea/vomiting, signs of raised ICP, seizures
Identify appropriate investigations for stroke (ischaemic and haemorrhagic) and interpret the results
Bloods
o Clotting profile - check if thrombophilia (especially in young patients)
ECG
o Check for arrhythmias that may be the source of the clot
Echocardiogram
o Identify cardiac thrombus, endocarditis and other cardiac sources of embolism
Carotid Doppler Ultrasound
o Check for carotid artery disease (e.g. atherosclerosis)
CT Head Scan
o Rapid detection of haemorrhages
MRI-Brain
o Higher sensitivity for infarction but less available
CT Cerebral Angiogram
o Detect dissections or intracranial stenosis
Generate a management plan for stroke (ischaemic and haemorrhagic)
HYPERACUTE STROKE
o If < 4.5 hrs from onset
o Exclude haemorrhage using CT-head
o If haemorrhage excluded, thrombolysis may be considered
ACUTE ISCHAEMIC STROKE
o Aspirin + Clopidogrel to prevent further thrombosis (once haemorrhage excluded on CT head)
o Heparin anticoagulation considered if there is a high risk of emboli recurrence or stroke progression
o Formal swallow assessment (NG tube may be needed)
o GCS monitoring
o Thromboprophylaxis
Secondary Prevention
o Aspirin and dipyridamole
o Warfarin anticoagulation (atrial fibrillation)
o Control risk factors: hypertension, hyperlipidaemia, treat carotid artery disease
Surgical Treatment - carotid endarterectomy
Identify the possible complications of stroke (ischaemic and haemorrhagic) and its management
- Cerebral oedema (increased ICP)
- Immobility
- Infections
- DVT
- Cardiovascular events
- Death
Summarise the prognosis for patients with stroke (ischaemic and haemorrhagic)
- 10% mortality in the first month
- Up to 50% that survive will be dependent on others
- 10% recurrence within 1 year
- Prognosis for haemorrhagic is WORSE than ischaemic
Define subarachnoid haemorrhage
• Arterial haemorrhage into the subarachnoid space
Explain the aetiology / risk factors of subarachnoid haemorrhage
- 85% - rupture of a saccular aneurysm at the base of the brain (Berry aneurysms)
- 10% - perimesencephalic haemorrhage
- 5% - arteriovenous malformations, bleeding diathesis, vertebral artery dissection
Risk Factors o Hypertension o Smoking o Excess alcohol intake o Saccular aneurysms are associated with: • Polycystic kidney disease • Marfan's syndrome • Ehlers-Danlos syndrome
Summarise the epidemiology of subarachnoid haemorrhage
- Incidence: 10/100,000
* Peak incidence: 40s
Recognise the presenting symptoms of subarachnoid haemorrhage
- Sudden-onset worst headache ever
- Nausea/vomiting
- Neck stiffness
- Photophobia
- Reduced level of consciousness
Recognise the signs of subarachnoid haemorrhage on physical examination
Meningism
o Neck stiffness
o Kernig’s sign
o Pyrexia
- GCS - check for deterioration
- Signs of raised ICP - papilloedema, IV or III nerve palsies, hypertension, bradycardia
- Focal neurological signs (e.g. cranial nerve palsies)
Identify appropriate investigations for subarachnoid haemorrhage and interpret the results
Bloods o FBC o U&Es o ESR/CRP o Clotting
CT Scan
o Hyperdense areas in the basal regions of the skull (due to blood)
Angiography - detect source of bleeding
Lumbar Puncture
o Increased opening pressure
o Increased red cells
o Xanthochromia - straw-coloured CSF due to breakdown of red blood cells
Define subdural haemorrhage
• A collection of blood that develops between the surface of the brain and the dura mater • Classification o ACUTE: < 72 hrs o SUBACUTE: 3- 20 days o CHRONIC: > 3 weeks
Explain the aetiology / risk factors of subdural haemorrhage
• Trauma (usually due to rapid acceleration and deceleration of the brain)
Summarise the epidemiology of subdural haemorrhage
- Acute - younger patients/associated with major trauma
- MORE COMMON than extradural haemorrhage
- Chronic - more common in the ELDERLY
Recognise the presenting symptoms of subdural haemorrhage
Acute
o History of TRAUMA with head injury
o Reduced conscious level
Subacute
o Worsening headache 7-14 days after injury
o Altered mental state
Chronic o Headache o Confusion o Cognitive impairment o Psychiatric symptoms o Gait deterioration o Focal weakness o Seizures
Recognise the signs of subdural haemorrhage on physical examination
Acute
o Reduced GCS
o Ipsilateral fixed dilated pupil (if a large haematoma cause a midline shift)
o Pressure on brainstem –> reduced consciousness + bradycardia
Chronic
o Neurological examination may be NORMAL
o Focal neurological signs (e.g. 3rd nerve palsy)
Identify appropriate investigations for subdural haemorrhage and interpret the results
- CT Head
* MRI Brain - higher sensitivity than CT
Generate a management plan for subdural haemorrhage
ACUTE
o ALS protocol
o Watch out for cervical spine injury
o If raised ICP consider osmotic diuresis
Conservative - if small
Surgical
o Prompt Burr hole or craniotomy
Chronic
o If symptomatic - Burr hole or craniotomy and drainage
Children
o Younger children may be treated with percutaneous aspiration via an open fontanelle
Identify the possible complications of subdural haemorrhage and its management
- Raised ICP
- Cerebral oedema
- Herniation
- Post-Op - seizures, recurrence, intracerebral haemorrhage, brain abscess, meningitis, tension pneumocephalus
Summarise the prognosis for patients with subdural haemorrhage
Acute
o Underlying brain injury will affect function
Chronic
o Better outcome than subdural haemorrhages
o Lower incidence of underlying brain injury
Define tension headache
• The most common type of headache, which is considered a ‘normal, everyday headache’.
• Can be divided into:
o Episodic - occurs on < 15 days per month
o Chronic - occurs on > 15 days per month
Explain the cause of tension headaches
• The exact cause is unclear • There are well-known triggers: o Stress/anxiety o Squinting o Poor posture o Fatigue o Dehydration o Missing meals o Bright sunlight o Noise • They are primary headaches (i.e. they have no underlying cause)
Summarise the epidemiology of tension headache
- MOST COMMON type of headache
- More common in WOMEN
- Most common in YOUNG ADULTS
- Most people will experience a tension headache at some point in their lives
Recognise the presenting symptoms and signs of tension headaches
- Mild-moderate in severity
- Pressure/tightness around the head like a tight band
- Pain tends to be bilateral
- Often a relationship with the neck
- Can be disabling for a few hours but does not have specific associated symptoms (unlike migraines)
- Gradual onset
- Variable duration
- Usually responsive to over-the-counter medication
- IMPORTANT: check for possible triggers when taking history (e.g. stress)
- Examination is usually NORMAL
Identify appropriate investigations for tension headaches
• NO investigations necessary
Generate a management plan for tension headaches
• Episodic Tension Headaches
o Reassurance
o Address triggers (e.g. stress, anxiety)
o Advice on avoiding medications that can cause medication-induced headaches (e.g. opioids)
o Simple analgesia (e.g. ibuprofen, paracetamol, aspirin)
o Tricyclic antidepressants may be considered in frequently recurrent episodic tension headaches or chronic tension headaches
Identify possible complications of tension headaches
• NONE
Summarise the prognosis for patients with tension headaches
- GOOD
- Not very severe or disabling
- Recurs
Define TIA
• Rapidly developing focal disturbance of brain function of presumed vascular origin that resolves completely within 24 hours.
Explain the aetiology/risk factors of TIAs
• It is usually EMBOLIC but may be thrombotic • Most common source of emboli = CAROTID atherosclerosis • Emboli can also arise from the heart: o Atrial fibrillation o Mitral valve disease o Atrial myxoma • NOTE: clots from the right side of the circulation can cause a stroke if there is a septal defect (e.g. PFO) • Risk Factors o Hypertension o Smoking o Diabetes mellitus o Heart disease (valvular, ischaemic, atrial fibrillation) o Peripheral arterial disease o Polycythaemia rubra vera o COCP o Hyperlipidaemia o Alcohol o Clotting disorders
Summarise the epidemiology of TIAs
- More common with increasing age
- More common in men
- 15% of stroke patients would have experienced a previous TIA
Recognise the presenting symptoms of TIAs
• ANY PATIENT presenting with acute neurological symptoms that resolve completely within 24 hours (i.e. a suspected TIA) should be given 300 mg aspirin immediately and assessed urgently within 24 hours
• History
o TIAs usually last 10-15 mins (but can be anything from a few minutes to 24 hours)
• Clinical features depend on the part of the brain affected:
o Carotid Territory
• Unilateral
• Most often affect the MOTOR AREA: weakness an arm, leg or one side of the face
• Dysarthria
• Broca’s dysphasia (if Broca’s area is involved)
• Amaurosis fugax (painless fleeting loss of vision caused by retinal ischaemia)
o Vertebrobasilar Territory
• Homonymous hemianopia (if ophthalmic cortex is involved)
• May be bilateral visual impairment
• May be hemiparesis, hemisensory symptoms, diplopia, vertigo, vomiting, dysarthria, dysphagia or ataxia
• Ask about weakness, facial drooping, gait disturbance, confusion, memory loss, dysarthria or abnormal behaviour
• Check for simultaneous cardiac symptoms (e.g. palpitations)
Recognise the signs of TIA on physical examination
- Neurological examination may be NORMAL because the TIA may have resolved by the time you do it
- Check pulse for irregular rhythm (AF)
- Auscultate the carotids to check for bruits (carotid atherosclerosis)
Identify appropriate investigations for TIAs
• Primary Care Investigations o Urinalysis (check for glycosuria) o FBC o U&Es o Lipids o LFTs o TSH o ECG (may show AF or previous MI) • Secondary Care o Unenhanced CT - if there is a possibility of a haemorrhage (e.g. if the patient is anticoagulated or has a bleeding disorder) • Investigate for Source of Emboli o ECG (24 hr tape or cardiac monitoring may be considered if paroxysmal atrial fibrillation is suspected) o Doppler ultrasound of carotid and vertebral arteries
Generate a management plan for TIAs
• Patients with acute neurological symptoms that resolve completely within 24 hrs should be given 300 mg aspirin immediately and assessed urgently within 24 hrs
• Patients with confirmed TIA should receive:
o Clopidogrel - 300 mg loading dose and 75 mg thereafter
o High-Intensity Statin Therapy - e.g. atorvastatin 20-80 mg
• Secondary Prevention
o Antiplatelets
o Antihypertensives
o Lipid-modifying treatments
o Management of AF
• Assessment of future stroke risk in TIA patients: ABCD2 score
Identify possible complications of TIAs
- Recurrence
* Stroke
Summarise the prognosis for patients with TIAs
• VERY HIGH RISK of STROKE in the first month after the TIA and up to 1 year afterwards
Define trigeminal neuralgia
• Neuralgia involving one or more of the branches of the trigeminal nerves, often causing severe pain.
Explain the aetiology/risk factors of trigeminal neuralgia
- Thought to be due to compression of the trigeminal nerve by a loop of artery or vein
- 5-10% of cases are thought to be due to tumours, MS or skull base abnormalities
Summarise the epidemiology of trigeminal neuralgia
- Peak incidence: 50-60 yrs
- Prevalence increases with age
- More common in FEMALES
- Some familial component
Recognise the presenting symptoms and signs of trigeminal neuralgia
• Sudden, unilateral, brief, stabbing pain in the distribution or one or more branches of the trigeminal nerve
• Recurrent
• Pain lasts from a few seconds to a couple of mins
• Periods of remission can vary
• Some experience preceding symptoms (e.g. numbness, tingling)
• Pain is described as being ‘shock-like’
• Triggers
o Vibration
o Skin contact
o Brushing teeth
o Oral intake
o Exposure to wind
Identify appropriate investigations for trigeminal neuralgia
- Diagnosis is CLINICAL
* If there is doubt over the underlying cause, specialists may request an MRI brain scan
Define Wernicke’s encephalopathy
• The presence of neurological symptoms caused by biochemical lesions of the central nervous system following exhaustion of vitamin B (particularly thiamine) reserves.
Explain the aetiology/risk factors of Wernicke’s encephalopathy
• Main cause is CHRONIC ALCOHOL CONSUMPTION which results in thiamine deficiency by causing:
o Inadequate nutritional thiamine intake
o Decreased thiamine absorption
o Impaired thiamine utilisation by cells
• Other conditions that cause thiamine deficiency:
o Chronic subdural haematoma
o AIDS
o Hyperemesis gravidarum
o Thyrotoxicosis
• Thiamine deficiency results in abnormal cellular function in the cerebral cortex, hypothalamus and cerebellum
Summarise the epidemiology of Wernicke’s encephalopathy
- Alcohol-related brain damage accounts for 10-24% of all dementia
- Prevalence rates are higher in areas of socio-economic deprivation
- Higher prevalence in 50-60 year olds
Recognise the presenting symptoms of Wernicke’s encephalopathy
- Vision changes: diplopia, eye movement abnormalities, ptosis
- Loss of muscle coordination: unsteady gait
- Loss of memory
- Inability to form new memories
- Hallucinations
Recognise the signs of Wernicke’s encephalopathy on physical examination
• Wernicke’s is classically defined by a triad of signs:
o Confusion
o Ophthalmoplegia
o Ataxia
• The patient is usually mentally alert with vocabulary, comprehension, motor skills, social habits and naming ability maintained
• Some show signs suggestive of polyneuropathy
• Reflexes may be decreased
• Abnormal gait and coordination
• Eye abnormalities on movement: nystagmus, bilateral lateral rectus palsy, conjugate gaze palsy
• Low temperature
• Rapid pulse
• Some may be cachectic
• NOTE: Korsakoff’s Psychosis occurs when the condition deteriorates further, leading to the additional symptoms of:
o Amnesia
o Confabulation
Identify appropriate investigations for Wernicke’s encephalopathy
• Diagnosis is mainly based on history and examination
• Possible useful tests:
o FBC (high MCV is a common feature amongst alcoholics)
o U&Es (exclude metabolic imbalances as a cause of confusion)
o LFTs
o Glucose
o ABG (hypercapnia and hypoxia can cause confusion)
o Serum thiamine
• CT head scan may be useful
