Neurology (2) Flashcards
Define multiple sclerosis
A chronic, relapsing-remitting demyelinating disorder caused by autoimmune destruction of myelin and oligodendrocytes in the CNS, leading to multiple transient neurological defects separated in space and time.
Summarise the aetiology of multiple sclerosis
Aetiology is unknown
Genetic factors - female, HLA-DR2
Environmental factors - infection, vitamin D deficiency
Autoimmune-mediated damage to myelin sheaths results in impaired axonal conduction
Risk factors: EBV exposure Prenatal vitamin D levels Autoimmune Disease Female Smoking
Summarise the epidemiology of multiple sclerosis
Most common in women
Age of presentation usually 20-40 years old
What are the presenting symptoms of multiple sclerosis?
Multiple transient neurological symptoms spread over space and time
Symptoms depend on where is affected
Charcot’s neurological triad - dysarthria, nystagmus, intention tremor
Optic neuritis:
Acute onset unilateral loss of visual acuity and colour perception with RAPD, preceded by pain
Sensory:
Parasthesia
Numbness
Burning
Motor: Ataxia Muscle weakness Spasm Stiffness Heaviness
ANS:
Constipation
Urinary incontinence
Depression
Psychosis
Lhermitte’s sign - electric shock down back and radiates to limbs when bending neck forwards
Uhthoff’s Sign: worsening of neurological symptoms as the body gets overheated from hot weather, exercise, saunas, hot tubs etc.
What are the signs on physical examination of multiple sclerosis?
Optic Neuritis:
Impaired Visual Acuity
Loss of colour vision
Relative Afferent Pupillary Defect - Both pupils contract (unaffected side) and both pupils dilate (affected side)
Fundoscopy: Swollen Optic Head (active disease) & Optic Atrophy (chronic disease)
Visual Field Testing: Central scotoma (blind sport in normal visual field if optic nerve is affected Field defects if optic radiations are affected
Internuclear Ophthalmoplegia:
Lateral horizontal gaze causes failure of adduction of the contralateral eye
Indicates lesion of the contralateral medial longitudinal fasciculus
Sensory: Paraesthesia
Motor: UMN signs
Cerebellar: Limb ataxia (intention tremor, past-pointing, dysmetria), dysdiadochokinesia, ataxic wide-based gait and scanning speech
What are the appropriate investigations for multiple sclerosis?
McDonald criteria = 2 or more CNS lesions with corresponding symptoms, separated in time and space
MRI head - paraventricular plaques (hyperintensities)
MRI spinal cord - demyelinating lesions
CSF - increased IgG, electrophoresis shows unmatched oligoclonal bands
Evoked Potentials - Visual, auditory and somatosensory evoked potentials may show delayed conduction velocity
Define encephalitis
Inflammation of the brain parenchyma leading to acute neurological dysfunction such as seziures, coma, personality changes, cranial nerve palsies, speech and motor problems.
Summarise the aetiology of encephalitis
Viruses most common: HSV - most common Enterovirus Varicella Zoster Virus Measles Mumps EBV Adenovirus Coxsackie HIV
Bacteria:
Listeria monocytogenes
Mycobacteria
Non-Viral causes (RARE): Syphilis, Staphylococcus aureus
In immunocompromised patients: CMV, Toxoplasmosis, Listeria
AI or Paraneoplastic: Associated with certain antibodies (e.g. anti-NMDA, anti-VGKC)
Summarise the epidemiology of encephalitis
No gender predominance
Age bimodal distribution - under 1 year old and over 65
What are the presenting symptoms of encephalitis?
SUBACUTE ONSET - HOURS TO DAYS Fever Headache Seizure Coma Drowsiness Fatigue Malaise Confusion Altered consciousness Altered brain function - personality changes Vomiting Meningism: Neck stiffness, photophobia Focal neurological symptoms (e.g. dysphagia, hemiplegia)
What are the signs on physical examination of encephalitis?
Reduced consciousness Deteriorating GCS MMSE may reveal cognitive/psychiatric disturbance Seizures Pyrexia/fever
Signs of Meningism:
Neck stiffness
Photophobia
Kernig’s test positive - lie supine, flex hip and extend knee causes pain
Signs of raised ICP:
Cushing’s Response: triad - hypertension, bradycardia, irregular breathing
Papilledema
Focal neurological signs (e.g. dysphagia, hemiplegia)
What are the appropriate investigations for encephalitis?
FBC - elevated WCC
Viral serology
MRI brain - increased intensities in frontotempr=oral region suggests HSV
CT - check for raised ICP
If no raised ICP - Lumbar puncture
CSF culture - high lymphocytes, increased monocytes and protein, normal glucose, elevated RBCs
Blood cultures
CSF PCR can show viral causes
Define stroke
An acute, permanent neurological deficit lasting >24 hours.
Summarise the aetiology of stroke
Ischaemic stroke - most common
Acute blockage of artery or critical stenosis of artery, preventing blood flow to brain
Thromobotic - atherosclerosis, fibromuscular dysplasia
Embolic - AF, atheroembolic, DVT passing through patent foramen ovale
Hypoxic - sepsis, infants, drowning
Hypotension
Haemorrhagic stroke: Burst blood vessel Intracerebral haemorrhage SAH - due to ruptured berry aneurysm Hypertension Amyloid angiopathy Arteriovenous Malformation Charcot Bouchard microaneurysm rupture (aneurysms within the brain vasculature that occur in small blood vessels)
What are the risk factors of stroke?
Ischaemic stroke RF: Hypertension Smoking Dislipidaemia Family history Increased age Diabetes AF Carotid artery stenosis
Haemorrhagic stroke RF: Increased age FHx Haemophilia Anticoagulation Hypertension Male
Summarise the epidemiology of stroke
Common
3rd most common cause of death in industrialised countries
Age 70+
What are the presenting symptoms of stroke?
Sudden onset Numbness Muscle weakness Visual disturbance Sensory or cognitive impairment Impaired coordination and/or consciousness Head or neck pain
What are the signs on physical examination of stroke?
Anterior Cerebral:
Lower limb weakness & Confusion
Middle Cerebral: Arms and face more than lower limbs Facial weakness Hemiparesis Hemisensory loss Apraxia Hemineglect (parietal lobe) Receptive or expressive dysphasia (Wernicke's and Broca's areas respectively) Quadrantopia (if superior or inferior optic radiations are affected)
Posterior Circulation: hemianopia, vertigo, ipsilateral ataxia, deafness, facial weakness
Intracerebral: headache, meningism, focal neurological signs, nausea/vomiting, signs of raised ICP, seizures
Initially: flaccid paralysis
Later: hyperreflexia, spastic paralysis
What are the appropriate investigations for stroke?
Bloods: FBC U&E’s Glucose Clotting profile (check if thrombophilia especially in young patients) Lipids Cardiac enzymes
ECG: Check for arrhythmias that may be the source of the clot (AF)
CT Head Scan: Distinguish between ischaemic and haemorrhagic stroke
MRI-Brain: Higher sensitivity for infarction but less available
Echo: Identify cardiac thrombus, endocarditis and other cardiac sources of embolism
Carotid Doppler Ultrasound: Check for carotid artery disease (e.g. atherosclerosis)
CT Cerebral Angiogram: Detect dissections or intracranial stenosis
What is the management of stroke?
Ischaemic:
<4.5 hours - CT head to exclude haemorrhage, thrombolysis with IV tissue plasminogen activator
> 4.5 hours:
Aspirin 300mg and clopidogrel - prevent further thrombosis
Swallow assessment
GCS monitoring
Heparin anticoagulation considered if there is a high risk of emboli recurrence or stroke progression (carotid dissection, recurrent cardiac emboli)
Thromboprophylaxis
Secondary Prevention - Aspirin and dipyridamole, Warfarin anticoagulation (AF)
Control risk factors:
Hypertension
Hyperlipidaemia
Treat carotid artery disease
Haemorrhagic stroke:
Surgery - clip or coil to block bleed
Craniotomy to reduce increased ICP
Nimodipine CCB
What are the possible complications of stroke?
Cerebral oedema (increased ICP) Immobility Infections DVT Cardiovascular events Death
Summarise the prognosis of stroke
10% mortality in the 1st month
Up to 50% survivors will be dependent
10% recurrence 1 year
Define motor neurone disease
Progressive neurodegenerative disease involving the motor cortex, anterior horn and cranial nerves, causing selective death and loss of neurones. It causes a combination of upper and lower motor neuron signs but NO sensory changes, sphincter disturbance or eye movement changes.
What are the types of motor neurone disease?
Amyotrophic lateral sclerosis - most common (80%)
Affects anterior horn and lateral corticospinal tract
LMN and UMN signs present
Muscle weakness, hyperreflexia, fasciculations, upgoing plantars, muscle atrophy
Progressive bulbar palsy
Affects cranial nerves IX - XII
Dysarthria, dysphagia, brisk jaw reflex, wasting and fasciculation of tongue
Progressive muscular atropy
LMN signs
Weakness, wasting, fasciculations, foot drop
Distal muscles affected first
Progressive lateral sclerosis
UMN signs
Spastic leg weakness
Summarise the aetiology of motor neurone disease
Unknown
Thought to be free radical damage and glutamate excitotoxicity
Genetic predisposition - SOD1 mutation on chromosome 21
Motor neurone degeneration
Summarise the epidemiology of motor neurone disease
Men affected more (3:2)
Average age of presentation 60 years old
5-10% have family history in autosomal dominant inheritence
What are the presenting symptoms of motor neurone disease?
Muscle weakness Muscle fasciculation Dysarthria Dysphagia Weak grip - difficulty turning door handle Weak shoulder abduction - difficulty washing hair Foot drop Proximal myopathy Stumbling spastic gait
What are the signs on physical examination of motor neurone disease?
UMN signs - hyperreflexia, spastic paralysis, weakness, upgoing plantars
LMN signs - weakness, fasciculations, atrophy, absent reflexes
What are the appropriate investigations for motor neurone disease?
No diagnostic investigation
EMG - denervation features
Nerve conduction - normal
Brain/spine MRI - exclude structural cause
Lumbar puncture - exclude infectious aetiology
Bloods - CK, ESR, anti-GMI ganglioside antibodies elevated
Define epilepsy
A tendency to recurrent, unprovoked and unpredictable seizures (a transient occurrence of signs and/or symptoms due to abnormal excessive or synchronous activity in the brain)
Types of seizures:
Partial - only affect part of the brain
Simple partial seizure - consciousness not affected
Complex partial seizure - consciousness affected
Generalised - affect both hemispheres and consciousness Atonic Tonic-clonic Myoclonic Absence Tonic Clonic
Summarise the aetiology of epilepsy
Increased excitation
Decreased inhibition
Idiopathic Secondary: Tumour Stroke Infection Injury Inflammation (MS, vasculitis) Toxic/Metabolic (sodium imbalance) Drugs (alcohol withdrawal, benzodiazepine) Vascular (haemorrhage, infarction) Malignant HTN or eclampsia Congenital abnormalities (cortical dysplasia) Neurodegenerative disease (Alzheimer's disease)
What are the risk factors of epilepsy?
Age (young & elderly) Family History Head Injury Stroke & Other vascular diseases Dementia Brain Infections Seizures in Childhood
Summarise the epidemiology of epilepsy
Common - 1% of population
Occurs in children and elderly
What are the presenting symptoms of epilepsy?
Partial Seizure Presentation:
Frontal Lobe Focal Motor Seizure: Motor convulsions, post-ictal flaccid weakness (Todd’s paralysis), Jacksonian March (spasm spreading from mouth/digit to ipsilateral side of face)
Temporal Lobe Seizures: Aura (visceral or psychic symptoms), Hallucinations (usually olfactory or affecting taste)
Frontal Lobe Complex Partial Seizure: Loss of consciousness, Involuntary actions/disinhibition, Rapid recovery
Generalised Seizures:
Tonic - sudden muscle stiffness, patient falls backwards
Atonic - sudden relaxation of muscles, patient falls forwards
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
Absence (Petit Mal): Onset in CHILDHOOD, Loss of consciousness but MAINTAINED POSTURE, patient appears stop talking, stares into space, NO post-ictal phase
Non-Convulsive Status Epilepticus: Acute confused state, often fluctuating, Difficult to distinguish from dementia
What are the signs on physical examination of epilepsy?
Tongue biting marks
Patients normal in between seizures
What are the appropriate investigations for epilepsy?
Bloods: FBC, U&E, LFT’s, Glucose, Calcium, Magnesium, ABG, Toxicology Screen, Prolactin (shows a transient increase shortly after ‘true’ seizure)
EEG: helps to confirm diagnosis & classify the epilepsy
3Hz waves - absence
Ictal EEGs are particularly useful
CT/ MRI shows structure, space occupying or vascular lesions
Other investigations: if suspected to be a secondary seizure i.e. due to infection – LP, HIV serology
What is the appropriate management of epilepsy?
STATUS EPILEPTICUS MX:
Seizure lasting >5 minutes of continuous seizure activity or repetitive seizures without regaining consciousness
ABC approach: resuscitate & protect airway, breathing and circulation
Check GLUCOSE (give glucose if hypoglycaemic) and consider thiamine
FIRST LINE = IV lorazepam OR IV/PR diazepam (benzodiazepine)
REPEAT again after 10 minutes if seizure doesn’t stop
If no response - IV phenytoin
If this also fails, consider general anaesthesia (e.g. thiopentone) – intubation and mechanical ventilation required
Treat the CAUSE (e.g. hypoglycaemia or hyponatraemia)
Check plasma levels of anticonvulsants (status epilepticus is often caused by lack of compliance with anti-epileptic medications)
Treatment of newly diagnosed epilepsy:
Start anti-convulsant treatment after > 2 unprovoked seizures
FOCAL Seizure 1st Line: lamotrigine or carbamazepine
GENERALISED Seizure 1st Line: sodium valproate
Absence = ethosuximide
Other anti-convulsant: phenytoin, levetiracetam, clobazam, topiramate, gabapentin, vigabatrin
Patient Education:
Avoid triggers (lack of sleep, stress, alcohol, changes in medication)
Use seizure diaries
Consideration for women of child-bearing age as AED’s can have teratogenic effects
Surgery may be considered for refractory epilepsy
What are the possible complications of epilepsy?
Fractures from tonic-clonic seizures
Behavioural problems
Sudden death in epilepsy
Complications of anti-epileptic drugs:
Gingival hypertrophy (phenytoin)
Neutropoenia and osteoporosis (carbamazepine)
Stevens-Johnson syndrome (lamotrigine)
Summarise the prognosis of epilepsy
50% Remission after 1 year
Mortality: 2 in 100,000/year directly related to seizure or secondary to injury
Define neurofibromatosis
An autosomal dominant condition affecting neural crest cells, resulting in multiple neurocutaneous tumours.
Neurofibromatosis type I - manifests with cafe-au-lait spots, painless cutaneous nodules, Lisch iris nodules, scoliosis, optic nerve gliomas
Neurofibromatosis type II - characterized by bilateral acoustic neuromas, bilateral juvenile cataracts and meningiomas
Summarise the aetiology of neurofibromatosis
Autosomal dominant condition causing defiency in tumour suppressor gene
Type I:
Mutation in NF1 gene of chromosome 17
Type II:
Mutation in NF2 gene of chromosome 22
Summarise the epidemiology of neurofibromatosis
Neurofibromatosis type I is more common
No gender or race predilection
What are the presenting symptoms of neurofibromatosis?
Type I: Multiple painless, mobile lumps under the skin (neurofibromas) Patches of milk-coffee coloured skin on back, buttocks and thigh Pain - peripheral nerve neurofibromas Learning difficulties Headache Visual changes - optic glioma Precocious puberty
Type II: Acoustic neuroma: Dizziness Bilateral tinnitus Bilateral gradual hearing loss
Catarcts:
Blurring of vision
Facial pain and Numbness
What are the signs on physical examination of neurofibromatosis?
Type I:
5 Cafe-au-lait spots >15mm diameter (>5mm in children)
Multiple small nodules under the skin (neurofibromas)
Lisch nodules - tan bumps on iris
Scoliosis
Freckling in armpit or groin
Type II:
Decreased sensorineural hearing
Catarcts
Facial nerve palsy/cerebellar signs (if schwannoma is large)
What are the appropriate investigations of neurofibromatosis?
MRI brain and spinal cord: for vestibular schwannomas, meningiomas and nerve root neurofibromas
PET: may demonstrate features compatible with optic pathway gliomas, other brain tumours, hydrocephalus, paraspinal neurofibromas, MPNST
Biopsy: histological features of a neurofibroma or MPNST (malignant peripheral nerve sheath tumour)
Genetic testing to confirm NF1 mutation
Ophthalmological assessment
Audiometry
Skull X-ray (sphenoid dysplasia in NF1)
Define subdural haemorrhage
Intracranial bleeding below the dura mater with slow bleeding, often following head trauma
ACUTE: < 72 hrs
SUBACUTE: 3- 20 days
CHRONIC: > 3 weeks
Summarise the aetiology of subdural haemorrhage
Rupture of branching veins in subdural space
Trauma due to rapid acceleration and deceleration of the brain
Rare: rupture of cerebral aneurysm OR vascular malformation
Risk factors: Elderly due to brain atrophy Children due to thin walled veins Alcohol abuse Trauma Anticoagulants
Summarise the epidemiology of subdural haemorrhage
More common than extradural haemorrhage
Acute cases = younger patients
Chronic cases = elderly
What are the presenting symptoms of subdural haemorrhage?
Usually delayed symptom onset due to low pressure veins Constant headache Trauma Vomiting Focal neurological symptoms Loss of consciousness Dementia-like symptoms
Acute: History of TRAUMA with head injury AND reduced conscious level
Subacute: Worsening headache 7-14 days after injury AND Altered mental state
Chronic: Headache, Confusion, Cognitive impairment, Psychiatric symptoms, Gait deterioration, Focal weakness, Seizures
What are the signs on physical examination of subdural haemorrhage?
Acute:
Reduced GCS
Ipsilateral fixed dilated pupil (if a large haematoma causes a midline shift)
Pressure on brainstem - reduced consciousness + bradycardia
Chronic:
Neurological examination may be NORMAL
Focal neurological signs (e.g. 3rd nerve palsy)
Cushing's signs of raised ICP: Bradycardia Hypotension Irregular respiration Papilloedema
What are the appropriate investigations of subdural haemorrhage?
CT head:
Crescent shaped hyperdensity that crosses suture lines
Hyperdensity = acute
Hypodensity or isodensity = chronic
Midline shift and ventricular compression when chronic
MRI scan: Subdural fluid collection. Higher sensitivity than CT especially for isodense or smaller subdural haematomas.
Plain skull x-ray: Not specific or sensitive for intracranial haematomas. Useful to identify possible skull fracture or presence of intracranial shrapnel.
What is the appropriate management for subdural haemorrhage?
ACUTE:
Advanced life support (ALS) protocol - cervical spine control & ABC
If signs of raised ICP: head elevation, osmotic diuresis (mannitol) and/or hyperventilation
Children: Younger children may be treated with percutaneous aspiration via an open fontanelle
Small (<10mm), no neurological signs, minimal midline shift (<5mm)- observation
Large and neurological signs - decompression surgery eg craniotomy
What are the possible complications of subdural haemorrhage?
Raised ICP Cerebral oedema Herniation Coma Stroke Neurological deficit Epilepsy
Post-Operation: Seizures (relatively common) Subdural haemorrhage Recurrence (up to 33%) Intracerebral haemorrhage Brain abscess Meningitis Tension pneumocephalus
Summarise the prognosis of subdural haemorrhage
Acute: Underlying brain injury will affect function
Chronic:
Better outcome than acute subdural haemorrhages
Reflects Lower incidence of underlying brain injury
Good outcomes in 75% of those treated with surgery
Define extradural haemorrhage
Bleeding between the skull and external dura mater
Summarise the aetiology of extradural haemorrhage
Trauma resulting in fracture of the temporal bone, resulting in rupture to the middle meningeal artery
Rarely: spontaneous
Risk factors: - Bleeding tendency i.e. haemophilia or anticoagulant therapy (warfarin)
Summarise the epidemiology of extradural haemorrhage
Common in adolescents and young adults following trauma, falls, assaults, RTAs
10% of severe head injuries
What are the presenting symptoms of extradural haemorrhage?
Loss of consciousness Period of lucency - asymptomatic Headache Vomiting Lethargy Neurological deficits Progressive deterioration in conscious level
What are the signs on physical examination of extradural haemorrhage?
Hypertension Wide pulse pressure Bradycardia Irregular respirations Scalp trauma or fracture to temporoparietal aspect of skull Headache Deteriorating GCS Signs of raised ICP i.e. dilated, unresponsive pupil on side of injury
What are the appropriate investigations for extradural haemorrhage?
Head CT:
Biconvex hyperdensity which does not cross suture lines, fracture, midline shift
Define spinal cord compression
Injury to the spinal cord with neurological symptoms depending on the site and extent of the injury and is a medical emergency
Summarise the aetiology of spinal cord compression and cauda equina syndrome
Spinal trauma - RTA, gunshot or knife wound, falls
Vertebral fracture - low energy fracture due to weakened bone
Disc herniation
Tumour - primary or metastatic
Infection - TB, discitis, epidural abscess
Cauda Equina: Lumbar disc herniation most common Spinal stenosis - congenital, ankylosing spondylitis Spondylolisthesis Tumour, cyst, abscess in spinal canal
Risk factors: Trauma Tumour Osteoporosis Metabolic Bone Disease Vertebral Disc Disease High Risk Occupation - construction workers, bricklayers High Risk Recreational Activities - vehicle racing, horse-riding IV Drug Use Immunosuppression
Summarise the epidemiology of spinal cord compression
Most common cause is trauma COMMON Trauma most common 16-30 Malignancy most common 40-75 Disc disease most common 30-50 Cauda equina: male aged 40-60 years
What are the presenting symptoms and signs on physical examination of spinal cord compression and cauda equina syndrome?
Spinal cord compression: Back pain Weakness Spastic paralysis Numbness or parasthesia Bladder or bowel incontinence Decreased anal sphincter tone Hyper-reflexia Sensory loss at lesion Priapism
Cauda equina syndrome: Saddle anaesthesia Weakness Flaccid paralysis Bladder and bowel incontinence Reduced or absent reflexes Decreased sexual function Back pain Sciatic pain Paraplegia
What are the appropriate investigations for spinal cord compression?
Radiology - Lateral radiographs of spine to look for loss of alignment, fractures
MRI or CT
FBC - raised WBC if infectious cause U&Es Calcium - bone mets ESR - raised if infectious cause Immunoglobulin electrophoresis (multiple myeloma)
Urinalysis - look for Bence Jones proteins (multiple myeloma)
Define meningitis
Inflammation of the leptomeninges (pia and arachnoid mater) most commonly caused by infection, resulting in a triad of headache, fever and nuchal rigidity.
Summarise the aetiology of meningitis
Bacterial: Neonates: Group B strep - long labour, infection in previous pregnancy E. coli - late neonatal infection Listeria monocytogenes
Children and teens:
Neisseria meningitides
Haemophilus influenzae - unvaccinated
Streptococcus pneumoniae
Elderly:
Streptococcus pneumoniae
Listeria monocytogenes - unpasteurised cheese/milk
Viral: coxsackie, enterovirus, HIV, HSV
Fungal: cryptococcus in immunocompromised eg HIV patients
Risk factors: Close communities (e.g. college halls) Basal skull fractures Mastoiditis Sinusitis Inner ear infections Alcoholism Immunodeficiency Splenectomy Sickle cell anaemia CSF shunts
Summarise the epidemiology of meningitis
Common in extremes of age
What are the presenting symptoms of meningitis?
Headache Fever Photophobia Phonophobia Neck pain/stiffness Non-blanching rash - only if caused by neisseria meningitides Vomiting
Infants: Lethargy Irritability Poor feeding Hypothermia High pitched crying
Confusion, mental state changes, change in consciousness, seizures if develops to meningoencephalitis
What are the signs on physical examination of meningitis?
Kernig’s sign - lie flat, lift leg and flex knee to 90 degrees, passive straightening of the leg causes back pain
Brudzinski’s sign - lie flat, passive flexion of the neck causes hips or knees to flex
Fever
Photophobia
Neck stiffness
Tachycardia
Hypotension
Buldging fontanelle in infants
What are the appropriate investigations for meningitis?
Blood culture - 2 sets
FBC - leukocytosis, anaemia
CRP - elevated
CT head to exclude raised ICP before LP
Lumbar puncture and CSF collection:
CSF glucose - decreased in bacterial and fungal
CSF protein - increased in all causes, largest increase in bacterial
CSF WBC - heavily elevated in bacterial with neutrophils, elevated with lymphocytes in viral and fungal
CSF PCR
CSF bacterial gram stain and culture
What is the management of meningitis?
IMMEDIATE IV Antibiotics (before LP)
First choice: 3rd generation cephalosporin - cefotaxime or ceftriaxone
Empiric for neonates - cefotaxime and ampicillin
Empiric teens - ceftriaxone, ampicillin, vancomycin
Benzylpenicillin may be used as an initial blind therapy
Dexamethasone IV - shortly before or with the first dose of antibiotics (reduces risk of complications)
What are the possible complications of meninigitis?
Septicaemia Shock DIC Renal failure Seizures Peripheral gangrene Elevated ICP Hearing loss Brain abscess Cerebral oedema Cranial nerve lesions Cerebral venous thrombosis Hydrocephalus Waterhouse-Friderichsen Syndrome (bilateral adrenal haemorrhage caused by severe meningococcal infection)
What is the prognosis of meningitis?
Mortality rate from bacterial meningitis: 10-40% with meningococcal sepsis
Viral meningitis is self-limiting
With prompt appropriate antimicrobial and supportive therapy good outcome
15% of children develop severe sequelae
Define raised intracranial pressure
Pressure inside the cranium exceeding 15mmHg, due to an increase in contents of the cranium due to the fixed volume
Summarise the aetiology of raised intracranial pressure
Primary or metastatic tumours Head injury Haemorrhage - subdural, extradural, subarachnoid Infection - meningitis, encephalitis, brain abscess Hydrocephalus Cerebral oedema Status epilepticus Idiopathic intracranial hypertension
Summarise the epidemiology of raised intracranial pressure
Idiopathic intracranial hypertension mainly in overweight women on childbearing age
What are the presenting symptoms of raised intracranial pressure?
Headache - worse in morning, on lying down, on coughing, straining, sneezing etc
Nausea and vomiting
Visual change - bilateral loss of vision momentarily on bending down, loss of peripheral fields
Seizures
Coma
Irritability
Drowsiness
What are the signs on physical examination of raised intracranial pressure?
Hypertension
Bradycardia
Cheyne-Stokes abnormal breathing - fast, deep breathing followed by period of apnoea
Decreased GCS - coma, irritability, seizures, drowsiness
Pupil constriction followed by dilation
What are the appropriate investigations for raised intracranial pressure?
FBC - infection
Glucose
Blood cultures - check for systemic infection
Toxicology screen - cause of decreased GCS
CXR - look for source of infection
CT head - may see haemorrhage, tumour, abscess, hydrocephalus etc
LP if no evidence of space occupying lesion
