Neuroscience Flashcards
What is Bell’s palsy?
An acute unilateral peripheral facial nerve palsy, consisting of deficits affecting all facial zones equally that fully evolve within 72 hours
What is the aetiology of Bell’s palsy?
Viral aetiology which is strongly associated with the herpes simplex virus (type 1)
What are the risk factors for Bell’s palsy?
Pregnancy (x3)
Diabetes (x5)
Intranasal influenza vaccination (no longer in clinical use)
What is the epidemiology of Bell’s palsy?
Bell’s palsy is the most common aetiology of unilateral facial palsy among those 2 years of age or older
Affects 15–40/100 000/yr
It is most prevalent in people between 15 and 45 years of age and equal in men and women
What are the presenting symptoms of Bell’s palsy?
Complete unilateral facial weakness
Quick onset (e.g. overnight or after a nap)
Ipsilateral numbness or pain around the ear
Reduced taste - anterior 2/3rds (ageusia)
Hyperacusis- hypersensitivity (from stapedius palsy)
Unilateral sagging of the mouth
Drooling of saliva
Food trapped between gum and cheek
Speech difficulty
Failure of eye closure may cause a watery or dry eye
What are the signs of Bell’s palsy on physical examination?
Unable to complete or resist on facial nerve actions
Unable to wrinkle their forehead (no forehead sparing which occurs in UMN lesions e.g. stroke) confirming LMN pathology
What are the appropriate investigations for Bell’s palsy?
1st Line:
-Clinical diagnosis: acute, unilateral facial palsy, with an otherwise normal physical examination
Rule out other causes:
-Blood: ESR; glucose; raised Borrelia antibodies in Lyme disease, raised VZV antibodies in Ramsay Hunt syndrome
- CT/MRI: Space-occupying lesions; stroke; MS
-CSF: (Rarely done) for infections.
What are the other causes of 7th nerve palsy?
Infective: Ramsay Hunt syndrome, Lyme disease, meningitis, TB, viruses (HIV, polio)
Brainstem lesions: Stroke, tumour, MS. Cerebellopontine angle tumours: Acoustic neuroma, meningioma
Systemic disease: DM, sarcoidosis, Guillain–Barré
Local disease: Orofacial granulomatosis, parotid tumours, otitis media or cholesteatoma, skull base trauma
What differentiates Lyme disease, Guillain–Barré, sarcoid, and trauma from Bell’s palsy?
They all often present with bilateral weakness
What is the management for Bell’s palsy?
Drugs:
-If given within 72h of onset, prednisolone speeds recovery, with 95% making a full recovery.
-Antivirals (eg aciclovir) can be used in the cases associated with HSV-1
Protect the eye:
-Dark glasses and artificial tears (eg hypromellose) if evidence of drying
-Encourage regular eyelid closure by pulling down the lid by hand
-Use tape to close the eyes at night
Surgery: Consider if eye closure remains a long-term problem (lagophthalmos) or ectropion is severe (eyelid turns outward)
What are the possible complications of Bell’s palsy?
Keratoconjunctivitis sicca: dry eye
Ectropion: sagging eyelid
Synkinesis: increased neural irritability and aberrant regeneration of motor axons e.g. eye blinking causes synchronous upturning of the mouth
Gustatory hyperlacrimation: (crocodile tears) misconnection of parasympathetic fibres can produce crocodile tears (gusto–lacrimal reflex) when eating stimulates unilateral lacrimation, not salivation
What is the prognosis for patient’s with Bell’s palsy?
Incomplete paralysis: without axonal degeneration usually recovers completely within a few weeks.
Complete paralysis: ~80% make a full spontaneous recovery, but ~15% have axonal degeneration in which case recovery is delayed
- Some evidence suggests pregnancy-associated Bell’s palsy is associated with worse long-term outcomes
What are central nervous system tumours?
Primary tumours arising from any of the brain tissue types
What is the aetiology of CNS tumours?
Children: most likely embryonic errors in development
Adults: unknown
What is the pathology of a meningioma?
Benign and most common primary CNS tumour
What is the pathology of a pituitary adenoma?
Benign, space-occupying and endocrine effects
What is the epidemiology of CNS tumours?
Annual incidence of primary tumours 5–9 in 100000 Two peaks of incidence (children and the elderly)
What are the presenting symptoms of CNS tumours?
Headache or vomiting (raised intracranial pressure)
Epilepsy (focal or generalized)
Focal neurological deficits (dysphagia, hemiparesis, ataxia, visual field defects, cognitive impairment)
Personality change
What are the signs of CNS tumours on physical examination?
Papilloedema / false localising signs (raised intracranial pressure)- bilateral hemianopia, anosmia, ophthalmoplegia
Focal neurological deficits (visual field defects, dysphasia, agnosia, hemianopia, hemiparesis, ataxia, personality change)
What are the appropriate investigations for CNS tumours?
CT-head: Usual initial investigation.
MRI-brain: Higher sensitivity.
Chest X-ray or CT (thorax, abdomen, pelvis): To determine if the lesion is secondary or primary.
Blood: CRP, ESR, consider HIV screen, toxoplasma serology (consider hormone profile-pituitary)
Brain biopsy: Type and grading (degree of differentiation of tumour)
*Lumbar puncture: contraindication if there is evidence of
raised intracranial pressure, may cause coning (herniation).
What is a cluster headache?
An attack of severe pain localised to the UNILATERAL orbital/supra-orbital and/or temporal areas.
Lasts between 15 minutes to 3 hours
Occurs from once every other day to 8 times per day
What is the aetiology of a cluster headache?
Unknown
What are the associated factors for a cluster headache?
History of head trauma
Heavy cigarette smoking
Heavy alcohol intake
What is the epidemiology for cluster headaches?
Affects men predominantly 2.5-3.5:1
What are the presenting symptoms for a cluster headache?
Repeated attacks of unilateral pain
Most patients are agitated and restless (only 7% can lie still during an attack)
Nausea and vomiting
Photophobia and phonophobia
Migraine type aura
Lacrimation, rhinorrhoea and partial Horner’s syndrome (ptosis and miosis: sympathetic features)
What are the signs of a cluster headache on physical examination?
Signs of Horner’s syndrome (ptosis and miosis)
What are the appropriate investigations for cluster headaches?
1st line: Brain CT scan or MRI Bloods-ESR Pituitary function tests Consider: ECG, polysomnogram (for sleep apnoea)
What is Encephalitis?
Inflammation of the brain parenchyma
What is the aetiology for Encephalitis?
In the majority of cases encephalitis is the result of a viral infection. Most common in the UK is HSV.
Other: bacteria (syphilis, staph A), immunocompromised (Cytomegalovirus, toxoplasmosis, Listeria)
What is the epidemiology of Encephalitis?
Annual UK incidence is 7.4 in 100,000
What are the presenting symptoms for Encephalitis?
Usually encephalitis is a mild self-limiting illness.
Subacute onset (hours to days) headache
Fever
Vomiting
Neck stiffness, photophobia, i.e. symptoms of meningism (meningoencephalitis) with behavioural changes
Drowsiness and confusion
There is often a history of seizures
Focal neurological symptoms (e.g. dysphasia and hemiplegia) may be present
It is important to obtain a detailed travel history
What are the signs of Encephalitis on physical examination?
Reduced level of consciousness with deteriorating GCS, seizures, pyrexia.
Signs of meningism: Neck stiffness, photophobia, Kernigs test positive.
Signs of raised intracranial pressure: hypertension, bradycardia, papilloedema.
Focal neurological signs.
Minimental examination may reveal cognitive or psychiatric disturbances.
What is Kernigs sign?
Positive when the thigh is flexed at the hip and knee at 90 degree angles, and subsequent extension in the knee is painful (leading to resistance)- indicating the presence of meningitis or subarachnoid haemorrhage
What are the appropriate investigations for Encephalitis?
Blood: FBC (raised lymphocytes), U&E (SIADH may occur), glucose (compare with CSF glucose), viral serology, ABG.
MRI/CT: Excludes mass lesion. HSV produces characteristic oedema of the temporal lobe on MRI.
Lumbar puncture: raised Lymphocytes,monocyte and protein, glucose usually normal. Viral PCR is first line.
EEG: May show epileptiform activity, e.g. spiking activity in temporal lobes
What is Epilepsy?
A chronic disorder that causes unprovoked, recurrent seizures (Paroxysmal synchronised cortical electrical discharges)
What are the two types of seizures?
Focal seizure:
-Seizure localised to specific cortical regions, such as temporal lobe seizures, frontal lobe seizures, occipital seizures, complex partial seizures
Generalised seizure:
Seizures which affect consciousness typically tonic-clonic, absence attacks, myoclonic, atonic (drop attacks) or tonic seizures
What is the aetiology of Epilepsy?
*The majority of cases are idiopathic
Primary epilepsy syndromes (e.g. idiopathic generalised epilepsy, temporal lobe epilepsy, juvenile myoclonic epilepsy)
Secondary seizures (symptomatic epilepsy):
-Tumour
-Infection (e.g. meningitis, encephalitis, abscess)
-Inflammation (vasculitis, rarely multiple sclerosis)
-Toxic/metabolic (sodium imbalance, hyper- or hypoglycaemia, hypocalcaemia, hypoxia, porphyria, liver failure)
-Drugs (e.g. including withdrawal e.g.alcohol, benzodiazepines)
-Vascular (haemorrhage, infarction)
-Congenital anomalies (e.g. cortical dysplasia)
-Neurodegenerative disease (e.g. Alzheimers disease)
-Malignant hypertension or eclampsia
-Trauma
What are common seizure mimics?
Syncope
Migraine
Non-epileptiform seizure disorder (e.g. dissociative disorder)
What is the epidemiology of Epilepsy?
Common
Prevalence in 1% of general population
Peak age of onset is in early childhood or in the elderly
What is the pathophysiology of Epilepsy?
Seizures result from an imbalance in the inhibitory and excitatory currents (e.g. Na+ or K+ ion channels) or neurotransmission (i.e. glutamate or GABA neurotransmitters) in the brain
What are the presenting symptoms of Epilepsy: Focal seizures?
Frontal lobe focal motor seizues:
Motor convulsions
May demonstrate Jacksonian march (spasm spreading from mouth or digit)
There may be post-ictal flaccid weakness (Todds paralysis)- on one side
Temporal lobe seizures:
Aura (visceral and psychic symptoms: fear or deja-vu sensation)
Hallucinations (olfactory, gustatory)
Frontal lobe complex partial seizures:
Loss of consciousness with associated automatisms and rapid recovery
May be postictal aphasia seen after focal-onset seizures
What are the presenting symptoms of Epilepsy: Generalised seizures?
Tonic-clonic (grand mal):
Vague symptoms before an attack (e.g. irritability), followed by tonic phase (generalised muscle spasm), followed by a clonic phase (repetitive synchro- nous jerks), and associated faecal or urinary incontinence, tongue biting
After a seizure, there is often impaired consciousness, lethargy, confusion, headache, back pain, stiffness
Absence (petit mal):
Usual onset in childhood
Characterized by loss of consciousness but maintained posture (patient stops talking and stares into space for seconds), blinking or rolling up of eyes with other repetitive motor actions (e.g. chewing)
No postictal phase.
Non-convulsive status epilepticus:
Acute confusional state
Often fluctuating
Difficult to distinguish from dementia.
What are the signs of Epilepsy on physical examination?
Depends on aetiology, usually normal between seizures
Look for focal abnormalities indicative of brain lesions
What are the appropriate investigations for Epilepsy?
Bloods:
- FBC: if raised WCC, may indicate an infectious cause
- U&E: electrolyte imbalance can lead to a provoked generalised tonic-clonic seizure
- Glucose: extreme hypoglycaemia or hyperglycaemia can cause provoked generalised tonic-clonic seizures
- Toxicology screen: identify cause
- Prolactin, helps to distinguish a generalised tonic-clonic seizure (GTCS) from a non-epileptic event (transient increase shortly after a true seizure)
- Creatinine Kinase (Elevated in true seizures)
EEG:
- Indicated after any unprovoked seizure event
- Helps confirm or refute the diagnosis; assists in classifying the epileptic syndrome: generalised epileptiform activity or focal, localising abnormality
- Usually performed inter-ictally and often normal and does not rule out epilepsy
CT/MRI:
For structural, space-occupying and vascular lesions
Other investigations: Particularly for secondary seizures according to suspected aetiology e.g. lumbar puncture (infections), HIV serology
What is the management of Epilepsy?
Only start anti-convulsant therapy after >2 unprovoked seizures:
- Lamotrigine: newer agent
- Topiramate: newer agent
- Oxcarbazepine
- Carbamazepine: reasonable choice
- Levetiracetam
- Valproic acid* contraindicated in pregnant women or women of a child bearing age
- Other medications: Phenytoin and Gabapentin
Patient education:
- Avoid triggers (e.g. alcohol)
- Encourage seizure diaries
- Recommend supervision for swimming or climbing, driving is only permitted if seizure free for 6 months
- Women of childbearing age should be counseled regarding possible teratogenic effects of AEDs and should consider taking supplemental folate to limit the risk
- Drug interactions: e.g. enzyme-inducing AEDs can limit the effectiveness of oral contraception
Surgery: limited for refractory epilepsy: Removal of definable epileptogenic focus
What is Status Epilepticus?
A life-threatening neurological condition defined as 5 or more minutes of either continuous seizure activity or repetitive seizures without regaining consciousness
What is the management for Status Epilepticus?
Treatment is often initiated in 5–10 minutes as early treatment has higher treatment success (definition is >30 mins)
1. Resuscitate and protect airway, breathing and circulation
2. Check glucose and give if hypoglycaemic- consider thiamine
3. IV lorazepam or IV or PR diazepam (repeat once after 15 min if needed)
If seizures recur or fail to respond, IV phenytoin (15mg/kg) under ECG monitoring
Alternative IV agents include phenobarbitone, levetiracetam or sodium valproate
4. If these measures fail, consider general anaesthesia. This requires intubation and mechanical ventilation
5. Treat the cause: e.g. correct hypoglycaemia or hyponatraemia
6. Check plasma levels of all anticonvulsants
What are the complications of Epilepsy?
Fractures with tonic-clonic seizures
Behavioural problems
Sudden death in epilepsy (SUDEP)
Complications of AEDs (e.g. neutropenia or osteoporosis with carbamazepine)
What is the prognosis of Epilepsy?
50% remission at 1 year
Mortality 2 in 100 000/year, directly related to seizure or secondary to injury
What is an Extradural Haemorrhage?
An acute bleed between the dura mater and the inner surface of the skull- also known as haematomas
What is the aetiology of Extradural Haemorrhage?
Most commonly caused by skull trauma in the temporoparietal area, usually following falls, assaults or sporting injuries
The pterion is vulnerable to trauma as it is the fusion point between the parietal, frontal, sphenoid and temporal bones: the middle meningeal artery is involved in 75% of EDH as it lies underneath the pterion, which leads to a high risk of arterial rupture
What is the epidemiology of Extradural Haemorrhage?
Patients most commonly affected are adult males between 20-30 years old because they are more likely to experience a traumatic injury
What are the presenting symptoms of Extradural Haemorrhage?
Early signs:
- Severe headache: occurs after the initial impact and can persist
- Initial loss or fluctuance in consciousness: may present vaguely as tiredness or confusion
-Period of lucidity after initial loss of consciousness: usually lasts between 6 and 8 hours but may last for days depending on the speed of the haematoma growth
Late signs:
Rapid deterioration and loss of consciousness:GCS score will begin to drop as intracranial pressure rises and the brainstem begins to herniate
What are the signs of Extradural Haemorrhage on physical examination?
Eyes:
- Focal neurological deficits become apparent in the eyes due to compression of the cranial nerves
- E.g. CNIII (oculomotor nerve) palsy may result in fixed dilation of the ipsilateral pupil. This is colloquially known as a “blown pupil”
Muscle weakness:
- Hemiparesis typically begins on the contralateral side to the EDH due to compression of the ipsilateral motor cortex
- Hemiparesis may become bilateral as the ICP increases and the brainstem becomes compressed
- Ipsilateral hemiparesis can also occur through Kernohan’s phenomenon (extensive midline shift of the brain due to mass effect from the growing extradural haematoma)
Upper motor neuron signs:
-Positive Babinski’s sign (upgoing toes), hyperreflexia and spasticity (hypertonia)
(signs are not specific to EDH)
Cushing’s triad:
A physiological response to critically high ICP
This is characterised by bradycardia, hypertension and deep/irregular breathing
Persisting unconsciousness: deep coma and very low GCS
Death: often by respiratory arrest
due to compression of the respiratory centres in the brainstem so they are unable to function
What are the appropriate investigations of Extradural Haemorrhage?
Non-contrast CT: FIRST LINE
- Show characteristic bi-convex mass within the skull if there is an EDH is present (“lemon-shaped” )
- Occurs as because the dura attaches to the skull more tightly across the suture lines and the pressure of the haematoma is not enough to overcome these sutures
- Secondary features on CT head can include midline shift and brain stem herniation, both of which are indications for early surgical intervention
MRI/X-ray: can also be performed but not as sensitive as CT. Show bone fractures and MRI can help differentiate between extradural and subdural haemorrhages through looking at the displaced dura
*Lumbar punctures are absolutely contraindicated for extradural haematomas, as they result in a drop in CSF pressure, which may speed up brain herniation
What is Guillain-Barré syndrome?
A type of acute inflammatory demyelinating polyneuropathy
What is the aetiology of Guillain-Barré syndrome?
An inflammatory process where antibodies after a recent infection reacts with self-antigen on myelin or neurons. Often no aetiological trigger is identified (idiopathic in about 40%), in other cases:
- Post-infection (1–3 weeks): bacterial (e.g. Campylobacter jejuni ), HIV, herpes viruses (e.g. zoster, CMV)
- Malignancy (lymphoma, Hodgkins disease)
- Post-vaccination
What is the epidemiology of Guillain-Barré syndrome?
nnual UK incidence is 1–2 in 100,000
Affects all age groups but rarely infants
Slight male predominance
What are the presenting symptoms of Guillain-Barré syndrome?
Progressive symptoms of 1 month duration of:
- Ascending symmetrical limb weakness (lower > upper)
- Ascending paraesthesia
Cranial nerve involvement (e.g. dysphagia, dysarthria and facial weakness)
In severe cases, the respiratory muscles may be affected
What are the signs of Guillain-Barré syndrome on physical examination?
General motor examination:
-Hypotonia
-Flaccid paralysis
-Arreflexia (typically ascending upwards from feet to head)
General sensory examination:
-Impairment of sensation in multiple modalities (typically ascending upwards from feet to head)
Cranial nerve palsies (less frequently):
Facial nerve weakness (lower motor neurone pattern)
Abnormality of external ocular movements
Signs of bulbar palsy
Autonomic function: Assess for postural BP change and arrhythmias
What is a severe sign of Guillain-Barré syndrome on physical examination?
Type II respiratory failure:
Important to identify early (e.g. CO2 flap, bounding pulse, drowsiness)
This can be insidious, and needs regular assessment
What are the appropriate investigations for Guillain-Barré syndrome?
Nerve conduction study:
Reduced conduction velocity or conduction block, but can be normal in the early phase of the disease
Lumbar puncture: elevated CSF protein, cell count and glucose normal
Blood: LFTs: elevation in hepatic enzymes
-Anti-ganglioside antibodies: present in 85% to 90% of patients with Miller-Fisher syndrome and 25% of
Guillain–Barre syndrome cases
Spirometry: reduced fixed vital capacity indicates ventilatory weakness, may also show reduced maximal inspiratory pressure, or maximal expiratory pressure
ECG: Arrhythmias may develop
What is Horner’s syndrome?
A disorder characterised by -pupillary miosis (constricted pupil) -ptosis (drooping of the upper eyelid) -facial anhydrosis (absence of sweating) This is due to the interference of the sympathetic trunk supplying the eye
What is the aetiology of Horner’s syndrome?
Usually due to the disruption of the sympathetic chain because of a lesion or a growth
Variety of factors:
-Carotid artery dissection
-Tumour in neck or chest cavity, particularly a neuroblastoma and a tumour of the upper part of the lung (Pancoast tumor)
-Lesion in midbrain, brain stem, upper spinal cord, neck, or eye orbit
-Inflammation or growths affecting the lymph nodes of the neck
-Surgery or other forms of trauma to the neck or upper spinal cord
What is the epidemiology of Horner’s syndrome?
Relatively rare disorder
The congenital, and more rare, form of Horner syndrome is present at birth
Affects everyone equally
What are the presenting symptoms of Horner’s syndrome?
Unilateral symptoms: Drooping upper eyelid Constriction of the pupil Dryness (lack of sweating) on the same side of the face (ipsilateral) as the affected eye Retraction of the eyeball
What are the signs of Horner’s syndrome on physical examination?
Pupillary miosis (constricted pupil) Ptosis (drooping of the upper eyelid) Facial anhydrosis (absence of sweating)
What are the appropriate investigations for Horner’s syndrome?
Drops e.g. tropicamide which will cause significant dilation of the healthy eye and little dilation of the affected eye if Horner syndrome is caused by a third-order neuron abnormality — a disruption somewhere in the neck or above
Imaging: locate the site of a probable abnormality causing Horner syndrome:
Magnetic resonance imaging (MRI): tumour in neck/lesion in brain
Carotid ultrasound: dissection
Chest X-ray: pancoast tumour at apex
CT: brain lesion/space occupying
Bloods: CRP/ESR inflammatory markers
What is the management for Horner’s syndrome?
No specific treatment, often resolves when an underlying medical condition is treated
In some cases surgical removal of the lesion or growth may be appropriate. Radiation and chemotherapy may be beneficial to patients with malignant tumours
What are the complications/prognosis of Horner’s syndrome?
Dependent on the underlying cause of Horner’s syndrome and it’s treatment
What is Huntington’s disease?
An autosomal dominant neurodegenerative disorder characterised by progressive chorea and dementia, typically commencing in middle age
What is the aetiology of Huntington’s disease?
Caused by an expanded CAG (extended trinucleotide repeat expansion) repeat at the N-terminus of the gene that codes for the huntingtin protein which results in toxic gain of function
The disease exhibits anticipation (earlier age of onset in each successive generation)
What is the epidemiology of Huntington’s disease?
Worldwide prevalence eight in 100 000
Average age onset 30–50 years, duration of disease is approximately 20 years from time of diagnosis to time of death
Affects men and women equally
Rare in East Asian populations (particularly Japan)
What are the presenting symptoms of Huntington’s disease?
FH of Huntingtons disease
Insidious onset in middle-age:
-Progressive fidgeting and clumsiness/restlessness
-Developing into involuntary, jerky, dyskinetic movements often accompanied by grunting and dysarthria
In late disease: the patient may become rigid, akinetic and bed-bound
Early cognitive, emotional and behavioural changes are dominated by lability (exaggerated changes in mood), dysphoria, mental inflexibility, anxiety, leading on to dementia
What are the signs of Huntington’s disease on physical examination?
Classically, patient presents with chorea and dysarthria
Slow voluntary saccades (quick simultaneous movement of both eyes) and supranuclear gaze restriction
Other presentations include:
-Parkinsonism and dystonia, muscles contract involuntary (especially in juvenile-onset disease)
-Mental state examination reveals cognitive and emotional deficits
What are the appropriate investigations for Huntington’s disease?
Genetic analysis:
Diagnostic if >39 CAG repeats in the HD gene
Imaging:
Brain MRI or CT may show symmetrical atrophy of the striatum (particularly the caudate nuclei) and butterfly dilation of the lateral ventricles
-not specific as it is seen in other conditions
Bloods:
May be necessary to exclude other pathology: anti-nuclear antibodies blood film (acanthocytes), TFT, ESR
What is Hydrocephalus?
The enlargement of the cerebral ventricular system (accompanied by raised CSF pressure)
Divided into:
Obstructive and non-obstructive
(or communicating or non-communicating)
What is the aetiology of Hydrocephalus?
Abnormal accumulation of CSF in the ventricles can be caused by:
(1) Impaired outflow of the CSF from the ventricular system (obstructive)
- lesions of the third ventricle, fourth ventricle, cerebral aqueduct
- posterior fossa lesions (e.g. tumour, blood) compressing the fourth ventricle
- cerebral aqueduct stenosis
(2) Impaired CSF resorption in the subarahnoid villi (non-obstructive)
- tumours;
- meningitis (typically tuberculosis)
- Normal pressure hydrocephalus (NPH) is the idiopathic chronic ventricular enlargement
* The long white matter tracts (corona radiata, anterior commisure) are damaged causing gait and cognitive decline
What is the epidemiology of Hydrocephalus?
Bimodal age distribution
In the young: congenital malformations and tumours
In the elderly: tumours and strokes
What are the presenting symptoms of Hydrocephalus?
Obstructive hydrocephalus: -Acute drop in conscious level -Diplopia (double vision) Normal Pressure Hydrocephalus (NPH): Chronic cognitive decline -Falls -Urinary incontinence
What are the signs of Hydrocephalus on physical examination?
Obstructive hydrocephalus: -Impaired GCS -Papilloedema -VI nerve palsy (false localizing sign of increased ICP) -In neonates, the head circumference may enlarge, and sunset sign (downward conjugate deviation of eyes) NPH: -Cognitive impairment -Gait apraxia (shuffling) -Hyper-reflexia
What are the appropriate investigations for Hydrocephalus?
CT head:
*-First-line investigation to detect hydrocephalus (ventricular enlargement)
-May also detect the cause (e.g. tumour in the brainstem)
CSF:
-Obtained from ventricular drains or lumbar puncture
-May indicate an underlying pathology (e.g. tuberculosis)
Check for MC&S, protein, glucose (CSF and plasma)
Lumbar puncture:
This is contra-indicated in obstructive hydrocephalus as it can cause tonsilar herniation and death
Others:
-Levodopa challenge: suspected Parkinsons due to gait apraxia
What is a lumbar puncture?
Also known as a spinous tap inserted between two vertebrae to remove a sample of cerebrospinal fluid
What are the indications for a lumbar puncture?
Diagnosis of CNS conditions/infections
Inject medications – such as painkillers, antibiotics or chemotherapy
Inject a spinal anaesthetic (epidural) – to numb the lower part of your body before an operation
Remove some fluid to reduce pressure in the skull or spine
What are the possible complications of a lumbar puncture?
A lumbar puncture is generally a safe procedure and serious side effects are uncommon.
Headaches
Swelling and lower back pain where the needle was inserted
Potential infections at site of insertion
What is Meningitis?
Inflammation of the meninges (pia mater and arachnoid) (coverings of the brain) most commonly caused by infection
What is the aetiology of Meningitis?
Infection:
Bacterial:
-Neonates: Group B streptococci, Escherichia coli, Listeria monocytogenes
-Children: Haemophilus influenzae, Neisseria meningitidis, Streptococcus pneumoniae
-Adults: Neisseria meningitidis (meningococcus), Streptococcus pneumoniae, TB
-Elderly: Streptococcus pneumoniae, Listeria monocytogenes
Viral: Enteroviruses, mumps, Herpes simplex V, HIV
Fungal: Cryptococcus (associated with HIV infection)
What are the risk factors for Meningitis?
Close communities (e.g. dormitories) Basal skull fractures Mastoiditis Sinusitis Inner ear infections Alcoholism Immunodeficiency Splenectomy Sickle cell anaemia CSF shunts Intracranial surgery
What is the epidemiology of Meningitis?
Variation according to geography, age, social conditions
Viral meningitis is one of the most common infections of the CNS
What are the presenting symptoms of Meningitis?
ASK ABOUT TRAVEL HISTORY *Severe headache *Photophobia *Neck stiffness or backache Irritability Drowsiness Vomiting Fever Clouding of consciousness High-pitched crying or fits (common in children)
