Neurology Flashcards

1
Q

Definition of Migraine & Types

A

A primary headache disorder, form of sensory processing disturbance with manifestations within & outside CNS function
A recurrent, moderate to severe headache commonly a/w nausea, photophobia & phonophobia.
The headache is typically unilateral and pulsating in nature lasting 4-72 hours.
There are two major types of migraine:
- Migraine without aura: characteristic migraine headache with associated symptoms.
Migraine with aura: a migraine headache that is preceded (and sometimes accompanied) by focal neurological symptoms.

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2
Q

Possible triggers/risk factors for Migraine

A
Stress
Caffeine intake
Menstruation 
Exercise 
Lack of Sleep
OCP
Certain foods e.g. chocolate
Family history
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3
Q

Clinical features of Migraine

A
Unilateral or bilateral throbbing/pulsating headache
Can be preceded by an aura
Visual changes
Moderate to severe pain
a/w nausea, photophobia, phonaphobia
wanting to sleep/sit in dark quiet room
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4
Q

Management of Migraine

A

Preventative measures - avoid triggers, keep diary, lifestyle advice
Acute - NSAID e.g. aspirin at aura, triptan at headache (sumatriptan), antiemetic e.g. metoclompromide
Preventative (if >2/month) - beta blockers, amitriptyline, topiramate, candasartan

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5
Q

Definition of Cluster Headaches

A

A severe primary headache disorder characterised by recurrent unilateral headaches centred on the eye or temporal region.

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6
Q

Clinical Features of Cluster Headaches

A

Unilateral severe headache
Autonomic sx – eye streaming, runny nose, conjunctival congestion, swelling of face/eyelids
Some patients can have night time attacks which will wake pt from sleep usually 2-6am
Severe agitation & restlessness
Periodicity

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7
Q

Investigations & Diagnosis of Cluster Headaches

A

Investigations:
Patients presenting with their first bout of a cluster-like headache should be referred to neurology for further review.
• Due to TACs being v common, patients should be referred to neurology as dx should be confirmed by specialist
Investigations typically consist of imaging to exclude sinister causes:
• MRI Brain
• CT Head

Diagnosis - clinical, dx by specialist

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8
Q

Management of Cluster Headaches

A

Aim to terminate acute attacks & prevent further ones
• Sumatriptan is often used first-line to terminate acute attacks (S/C or intranasally)
• Short burst oxygen therapy: 100% oxygen (12-15L/min) can be administered via a non-rebreather face mask for 15-20 minutes
• Avoid triggers e.g. alcohol, smoking

Traditional analgesic medications like paracetamol, opiates and NSAIDs are not recommended.

Preventative (long term) - verapamil (high dose, ECG monitoring), topiramate

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9
Q

Definition of Trigeminal Neuralgia & Clinical Features

A

Sudden, severe facial pain, often described as a sharp shooting pain or like having an electric shock in the jaw, teeth or gums (within the distribution of the trigeminal nerve).

Short-lived episodes of electric shock pain in the distribution of the trigeminal nerve
Usually unilateral (>97%)
Recurrent attacks - triggers inc cold air, eating

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10
Q

Aetiology of trigeminal neuralgia

A

Primary trigeminal neuralgia
• Refers to disease caused by vascular compression - thought to account for 80-95% of cases
• This normally occurs near the root of the nerve at the ‘nerve root entry zone’
• The compression is thought to lead to demyelination and abnormal electrical activity in response to stimuli

Secondary trigeminal neuralgia
• Refers to disease occurring secondary to another condition
• Compression may be caused by other lesions (e.g. vestibular schwannoma, meningioma, cysts)
• Multiple Sclerosis

Idiopathic trigeminal neuralgia

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11
Q

Management of Trigeminal Neuralgia

A

Consider urgent ref for MRI if sinister cause suspected
1st line - carbamazepine 100mg BD & titrate upwards until remission
2nd line - gabapentin or lamotrigine

Surgical options - microvascular decompression or gamma knife radiosurgery

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12
Q

Definition & Risk factors for Idiopathic intracranial hypertension

A

A disorder caused by chronically elevated intracranial pressure (ICP), which leads to the characteristic clinical features of headache, papilloedema (swollen optic discs) and visual loss.

Weight (obesity), age (reproductive age) & sex (female)

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13
Q

Clinical features of IIH

A

Headache - worse on lying down, bending forwards & in the morning
Visual changes - transient vision loss, flashes of light, diplopia
Tinnitus
Neck/back pain
pain behind eyes

papilloedema
6th nerve palsy

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14
Q

Investigations for IIH

A
Obs (BP)
Urinalysis - pregnancy & renal disease
Bloods
Opthalmoscopy 
MRI (R/O other causes)
LP - measure pressures
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15
Q

Differentials for IIH

A

SOL, venous sinus thrombosis, obstructive hydrocephalus, decreased CSF reabsorption or increased CSF production

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16
Q

Management of IIH

A

Weight loss
• Low sodium weight loss plan
Serial LPs
Occasionally may be offered to remove excess CSF
Pharmacotherapy
• carbonic anhydrase inhibitor (e.g. acetazolamide) is the treatment of choice for IIH
• Thought to work by reducing amount of CSF production
Surgical
• Optic nerve sheath fenestration
Shunting

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17
Q

Clinical Features of Tension Type Headache

A

Classically they produce a mild ache across the forehead and in a band-like pattern around the head.
This may be due to muscle ache in the frontalis, temporalis and occipitalis muscles. Tension headaches comes on and resolve gradually and don’t produce visual changes.

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18
Q

Risk factors/associations for tension type headaches

A
Stress
Depression 
Dehydration
Alcohol
Skipping meals
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19
Q

Red Flags in Headaches

A

Headache Characteristics - severe sudden onset, progression or acute changes, worse on standing/lying down

Precipitating factors - recent trauma (subdural), triggered by Valsalva manoeuvre

Associated features -
fever/photophobia/neck stiffness (meningitis), papilloedema (IIH, SOL, CVS), vomiting (SOL, CO poisoning), dizziness/vertigo (stroke), visual changes (GCA, glaucoma)

Patient factors - age >50 or <10, immunodeficiency, active or previous cancer, pregnancy

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20
Q

Management of Tension Headaches

A

Analgesia: Simple painkillers such as paracetamol of NSAIDs (if no contra-indications), to be taken when headache occurs.

Lifestyle: Evaluate and offer help with possible precipitants. Consider sources of stress, depression/anxiety, sleep disorder and chronic illnesses. Some patients find regular exercise helps.

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21
Q

Medication-Overuse Headaches; definition & management

A

Medication ‘overuse’ itself has been shown to result in chronic headaches.
As the name suggests this occurs when regular analgesia taken for symptomatic relief of headache causes or perpetuates the condition.

It gives similar non-specific features to a tension headache.

Stop/reduce medications within a month - may get worse before better

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22
Q

Definition & Aetiology of Subarachnoid Haemorrhage

A

Arterial haemorrhage/bleeding into subarachnoid space (bet arachnoid & pia mater)

Traumatic - HI
Spontaneous - aneurysm rupture, AVM, rarer (CA dissection)

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23
Q

Risk factors for SAH

A

Hypertension
Smoking
Alcohol
Substance/drug abuse e.g. cocaine, amphetamines
Sex - higher risk in females
Race: higher incidence in Japanese/Finnish populations
Family history of aneurysms

Genetic predisposition
○ autosomal dominant polycystic kidney disease (increased tendency to form berry aneurysms) or type IV Ehlers-Danlos syndrome

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24
Q

Clinical features of SAH

A
Sudden severe thunderclap headache
Photophobia & neck stiffness
N&V
Visual changes - ptosis, 3rd nerve palsy, diplopia 
Reduced GCS
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25
Investigations & Management of SAH
Observations & Examination, Bloods inc G&S, clotting, Imaging (CT head) If CT head normal - LP in 12hrs (detect bilirubin) Initial management - A to E survey, ?airway management if needed Medical - analgesia, anti-emetics, IV fluids & monitoring, regular neurological observations, nimodipine Surgical/aneursym management - coiling/clipping
26
Definition & Aetiology of Subdural Haemorrhage
Rupture of bridging veins, bleeding between dura & surface of brain acute - within 72hrs, subacute 3-20days, chronic after 3 weeks Usually caused by trauma (fall, HI) but can be caused by aneurysm rupture, AVM etc RFs: elderly, alcoholics, anticoagulated, HTN, presence/hx of aneurysms
27
Clinical features of Subdural Haemorrhage
History of trauma & HI with decreased level of consciousness (ACUTE) Worsening headaches for 7-14days after injury, altered mental state (SUBACUTE) Headache, fluctuating confusion, cognitive impairment, focal weakness, seizures (CHRONIC) ``` Seizures Weakness Vomiting Reduced consciousness Sudden neurological sx ```
28
Investigations for subdural haemorrhage
Urgent CT head - confirm diagnosis, crescent shaped • History/examination/observations - inc neuro examination, pupils & A-E survey • Bloods - FBC (Hb, plt), U&Es, LFTs (alcohol), clotting, G&S, bone profile • Imaging - CT head ○ Crescent shaped ○ Acute subdural bleeds = hyperdensity = paler Chronic subdural bleeds = hypodense = darker
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Management of Subdural Haemorrhage
Management: Initial A to E survey; C spine, D inc pupil check & GCS, signs of raised ICP Conservative If small & minimal midline shift Closely monitor with neuro obs, manage & prevent ICP Ensure normal sats, normal temp, normal CO2, adequate sedation and paralysis, ICP monitoring Seizure management Surgical Stopping bleeding/evacuation of chronic subdurals Burr Holes
30
Definition & Aetiology/RFs - Extradural Haemorrhage
Bleeding into extradural space - above dura mater Trauma - high impact, high energy trauma Causes temporal/parietal bone fracture which leads to damage/tear of MMA ``` Mechanism of Injury Anticogulation/antiplatelet use Alcohol excess Liver dysfunction Coagulopathy ```
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Clinical Features - Extradural Haemorrhage
``` · History of trauma, brief LOC followed by a lucid interval · Headache · Nausea & vomiting · Seizures Speech difficulties ``` ``` • Reduced GCS/consciousness • Confusion • Focal neuro deficits • Unequal pupils • Herniation CSF leak ```
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Investigations for Extradural Haemorrhage
Plain CT head - shows blood in extradural space, forms lemon shape, midline shift • Bedside; neuro obs & examination, history, BM & ECG • Bloods; FBC (Hb, plt), U&Es, LFTs (alcohol), clotting, G&S, CM, bone profile Imaging; CT head +/- full trauma screen e.g. whole body CT
33
Management of Extradural Haemorrhage
``` Trauma call & primary survey Any resuscitation that is appropriate Admit to HDU Discuss with specialist neuro team Surgery - decompression ```
34
Definition & Types of Multiple Sclerosis
Chronic, immune mediated, neuroinflammatory condition which involves demyelination of central nervous system (UMN) Relapsing-remitting Primary progressive MS Secondary progressive ms
35
Risk factors/aetiology - MS
• Genetics ○ Increased risk if family hx ○ Twins - 1 in 5, if identical twin is affected --> shows GxE • Vit D levels ○ Live further away from the equator = increased risk ○ Patients with MS have lower Vit D levels - ?cause vs effect ○ Some genetic components linked to development of MS & involved in Vit D • Viral - EBV prevalance • Obesity Sex - female
36
Clinical features of MS
``` Visual Symptoms • Optic neuritis - unilateral deterioration visual acuity & colour perception, pain on eye movement • Blurred vision Motor symptoms + UMN symptoms on examination • Limb weakness • Spasms • Stiffness & heaviness Sensory symptoms • Pins & needles • Numbness • Burning Autonomic • Urinary urgency • Hesitancy • Incontinence • Impotence ```
37
Management of MS
• Acute attacks - high dose steroids e.g. Methylprednisolone 500mg PO for 5/7 ○ Although will get better on own, steroids quicken recovery Preventing relapses - beta interferon, DMARDs
38
Definition of Parkinson's Disease
Neurodegenerative disease - loss of DAnergic neurones within substantia nigra (basal ganglia)
39
Clinical Features of Parkinson's Disease
Bradykinesia, rigidity, resting tremor & postural instability Mask-like expression, micrographia, shuffling gait, gabellar tap
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Genetic Factors in Parkinson's Disease
``` SNCA DJ-1 - support/chaperone LRRK2 - mutations inhibit autophagy PINK1 PARKIN ```
41
Investigations & Diagnosis - Parkinson's Disease
Clinical diagnosis - history & examination DX by specialist using criteria DAT scan - reduced MRI/CT - r/o other pathologies Bloods - serum ceruloplasmin to r/o Wilson's Disease in young onset Levodopa trial
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Differentials for Parkinson's Disease
Essential tremor - intention tremor, symmetrical Progressive supranuclear palsy Multiple systems atrophy - autonomic sx Dementia with Lewy Body - LBD cognitive symptoms within one year of motor features.
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Management of Parkinson's Disease
Medical - symptomatic therapy with DA replacement • L-DOPA - levodopa + carbidopa (peripheral DOPA decarboxylase inhibitor) • DA agonists - ropinirole • MAO inhibitors - selegiline • COMT inhibitors - entacapone Surgical • Deep Brain stimulation
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Defintion/Criteria for Epilepsy
A chronic neurological disorder which is characterised by recurrent seizures Criteria 1: ≥2 unprovoked (or reflex) seizures occurring more than 24 hours apart Criteria 2: 1 unprovoked (or reflex) seizure with a probability of further seizures felt to be at a similar recurrence risk to patients with ≥2 unprovoked seizures over the next 10 years. Criteria 3: A diagnosed epilepsy syndrome
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Classification of Epilepsy
Based on seizure type, epilepsy type & syndrome Seizure type - onset(focal/generalised), awareness, clinical features Epilepsy type - focal, generalised, both or unknown Syndrome - can be classified into syndromes based on further findings e.g. onset age, EEG findings
46
Risk factors for Epilepsy
• Cerebrovascular disease • Head trauma • Cerebral infections • Family history: epilepsy or neurological illness • Premature birth • Congenital malformations of the brain Genetics conditions associated with epilepsy
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Differentials - epilepsy mimics
syncope, pseudoseizures, migraine associated disorders, paroxysmal movement disorders, sleep disorders
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Investigations for Epilepsy
* ECG * Bloods: FBC, U&E, LFT, Glucose, Bone profile * Other: depending on suspected aetiology and age of presentation * EEG * MRI Brain
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Management of Epilepsy & Important Considerations
Patient Education & Safety Anti-epileptics - focal (lamotrigine-carbamazepine), generalised (sodium valproate - lamotrigine) Other options inc: Levetiracetam, Phenytoin * women of child bearing ages - sodium valproate * interactions of contraception - CYPP450
50
Definition of Status Epilepticus
Continuous epileptic activity which failed to self terminate - lasting >5mins In SE there is prolonged seizure activity either due to failure of the mechanisms responsible for seizure termination, or from the initiation of mechanisms which lead to abnormally prolonged seizures
51
Causes of status epilepticus
``` ® Part of epilepsy syndrome ® Hypoglycaemia ® Infection (meningitis/ encephalitis) ® Intracranial haemorrhage ® Electrolyte imbalance (hypo/hyper Na+, Ca2+) ® Drug-related · withdrawal – benzodiazepines, opioids · toxicity – tricyclic antidepressants ```
52
Management of Status Epilepticus
· Pre-hospital: PR Diazepam (10-20mg) repeat 15mins if continuing or give buccal midazolam 10mg · Primary survey; protect airway, breathing & circulation · Check glucose & respond accordingly Next steps: IV lorazepam  phenytoin infusion  GA General principles of management (for us) ® ABCDE ® 2x Benzodiazepines + Call a senior doctor ® Phenytoin / phenobarbitone Rapid sequence induction
53
Definition & Types of Encephalitis
Inflammation of brain parenchyma Infectious - viral (HSV), bacterial, fungi Non-infectious - AI, paraneoplastic & post infectious
54
Aetiology of Encephalitis
``` • Infectious (common) ○ Herpes Simplex Virus (HSV) ○ Others include: arboviruses (e.g. West Nile virus), varicella-zoster virus, Epstein-Barr virus, and human immunodeficiency virus (HIV) ○ Bacterial causes - mycoplasma, TB ○ Fungi - histoplasmosis ○ Parasites ``` • Non-infectious ○ Paraneoplastic ○ Post-infectious ○ Auto-immune (NMDA & VGKC)
55
Clinical features of encephalitis
Classic presentation - new onset fever, headache & altered mental state +/- focal neurological deficits Can be highly variable dependent on underlying cause & area of brain that was been affected fever, headache, seizures, altered mental status, behavioural changes
56
Investigations for encephalitis
• Bedside - observations, urinalysis, ECG & sputum cultures ○ Mostly to r/o other causes of infection e.g. UTI • Bloods - FBC, U&Es, bone profile, LFTs, CRP, cultures & coagulation • Imaging - CXR & CT head/MIR r/o stroke, SOL ``` More specialist: • Neuroimaging • EEG • CSF analysis (Lumbar Puncture) - CT first if worried about SOL Serological testing - antibodies ```
57
Management of encephalitis
Principle treatment of HSV encephalitis is IV aciclovir * HSV encephalitis --> IV aciclovir * Antimicrobials or antivirals directed to cause * Immunosuppressive therapies (e.g. steroids) can be used to treat paraneoplastic, autoimmune, and post-infective causes but it is essential an infection is excluded before these are initiated.
58
Definition & Pathophysiology of Guillian Barre Syndrome
Acute inflammatory demyelinating polyneuropathy affecting PNS - progressive &ascending Immune mediated
59
Aetiology of Guillian Barre Syndrome
• Idiopathic (40%) • Post-infection (1-3 weeks) ○ Bacterial - campylobacter jejuni *most common identifiable trigger* ○ HIV ○ Herpes Simplex • Malignancy (lymphoma, Hodgkin's Disease)
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Clinical Features of Guillian Barre Syndrome
Progressive symptoms of <1mth duration of: - Ascending symmetrical limb weakness (lower>upper) - Ascending paraesthesia May have a history of recent illness e.g. D&V, gastroenteritis Examination: Motor - hypotonia, flaccid paralysis, areflexia Sensory - impaired in multiple modalities
61
Differentials for Guillian Barre Syndrome
Differentials: Lyme disease, sarcoidosis, thiamine deficiency, porphyria and neoplasms
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Investigations for GBS
The diagnosis of GBS is suspected based on the clinical presentation. Investigations aim to confirm a diagnosis of GBS and exclude differentials. Specialist investigations needed: lumbar puncture & nerve conduction studies
63
Management of Guillian Barre Syndrome
Acute: high dose IV immunoglobins or plasmapheresis may reduce duration or severity Supportive: airway & cardiac monitoring, DVT prophylaxis, long term recovery help e.g. OT, physio
64
Brown-Sequard Syndrome - aetiology, pathology, S&S, investigations
Condition a/w hemisection of the spinal cord, characterised by loss of temperature, pain, touch on one side (spinothalamic - sensory, contralateral) & paralysis on the other (corticospinal - motor, same side, iplatera) `Causes; Spinal fractures, Gunshot wounds, Stab wounds, Crush injury, Inflammatory diseases, Tumours, Vertebral disc herniation, Vascular reasons include hemorrhage or ischemia. Diagnostic imaging - MRI ****EXAMPLE: R side of spine taken out - loss of sensory on L side & motor loss on R*****
65
Describe a 3rd Nerve Palsy
Down & Out eye fixed & dilated pupil ptosis Causes include: aneurysm of posterior communicating artery, infarction of nerve (diabetes), midbrain infarction or tumour
66
Define myotome & dermatome
Dermatome - area of skin supplied by single spinal nerve (sensory) Myotome - group of muscles innervated by single spinal nerve (motor)
67
Myotome actions of Upper Limb
C4 - ''shrug shoulders'' C5 - shoulder ABduction, (elbows out & stop me from pushing them down), boxers pose (stop me from pulling them out) C6 - shoulder aDDuction, (elbows out & stop me from pushing up), boxers pose (stop me from pulling them out), wrist flexion C7 - elbow extension (boxers pose & push against me), wrist flexion C8 - thumb ABduction (thumbs to sky & stop me from pushing them down) T1 - finger ABduction (index finger, stop me pushing it in)
68
Myotomes of Lower Limb
L2 - hip flexion (raise leg up to sky) *L5/S1 - hip extension (push down into bed)* L3 - knee extension (try & straighten leg) *S1 - knee flexion* L4 - ankle dorsiflex (upwards) L5 - big toe extension S1 - ankle plantar flex (pedal)
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Reflexes - Upper Limb
Triceps - C7 Biceps - C5/C6 Supinator - C5/C6
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Reflexes - Lower Limb
Knee jerk - L3/L4 ''kick the door'' Ankle jerk - S1 Plantar - L5/S1
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Meningitis - define, causes, S&S, ix & management
Definition: Inflammation of the meninges - outer membranes covering brain & spinal cord Aetiology & Risk factors: Can be due to number of infectious (viral vs bacterial) & non-infectious causes Bacterial Meningitis • Bacterial - Neisseria meningitidis (meningococcus, gram -ve diplococcus) ○ Meningococcal septicaemia - bacterial infection has entered bloodstream § Cause of classic non-blanching rash, indicated DIC & subcutaneous haemorrhages ○ Meningococcal meningitis - in the brain • Bacterial - Streptococcus pneumoniae • Bacterial (neonatal) - Group B Streptococcus ○ Usually contracted during birth from GBS vaginal bacteria Viral Meningitis - tends to be milder & often only requires supportive treatment. Aciclovir can be used to treat suspected or confirmed HSV meningitis • Herpes simplex virus (HSV) • Enterovirus • Varicella zoster virus (VZV ``` Presentation/Clinical Features: Signs & Symptoms • Fever • Neck stiffness • Vomiting • Headache • Photophobia • Altered consciousness • Seizures • Non-blanching rash (meningococcal septicaemia) ``` O/E - Kernig's test & Brudzinski's test In Neonates • Hypotonia • Poor feeding • Lethargy • Bulging fontanelle • Hypothermia • LP should be performed in all children: ○ Under 1 months presenting with fever ○ 1 – 3 months with fever and are unwell ○ Under 1 years with unexplained fever and other features of serious illness Investigations & Diagnosis: Bedside/Community • ABCDE - if critically unwell • Focused history: ○ important to determine any preceding illnesses that increase risk of meningitis (e.g. sinusitis, otitis media, contact with an affected patient) • Allergy status • Formal examination ○ assess for meningeal irritation, look for non-blanching rash and signs of sepsis (e.g. hypotension, tachycardia) • Throat Swab • Respiratory viral screen (nasopharyngeal swab) • STAT IM BENZYLPENICILLIN DOSE (1200 mg - adults, age adjusted for children) ``` Bloods • FBC, U&Es, LFTs, bone profile, coagulation, CRP • Blood cultures • Venous blood gas • Meningococcal PCR ``` Imaging • CT head - usually done as part of work up, normally to r/o any contraindications for an LP ○ Some indications e.g. immunocompromised patient, hx of CNS disease, new onset seizures etc Special Tests • LUMBAR PUNCTURE (L3/L4)- every patient w/ suspected meningitis should undergo an LP & CSF evaulation ○ Ideally before abx, however difficult to implement in practise ○ Looks at: cell count & differential, protein, glucose, MC&S, viral PCR, save sample ○ May be able to isolate pathogen to tell if viral vs bacterial, but can also look at results of CSF § Bacterial = v high WCC, normal/reduced glucose & neutrophils § Viral = high WCC, normal glucose & lymphocytes Management: Depends on aetiology - usually treated for bacterial meningitis as really don't want to miss it Bacterial • 1st line = ceftriaxone (3rd gen cephalosporin) ○ It should be used with caution in patients with penicillin allergy due to cross-reactivity ○ If there is a severe penicillin allergy (e.g. anaphylaxis) it should be avoided. • 2nd line = chloramphenicol Viral • Majority secondary to enterovirus & don't require any specific treatment • Supportive measures inc rest, hydration, analgesia & anti-pyretic agent • Aciclovir used if concern of encephalitis or HSV infection
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Pathophysiology of movement disorder - MS, MG, MND
Multiple Sclerosis - autoimmune T cell mediated chronic demyelination in CNS, occurs sporadically throughout brain & spinal cord, lesions must be disseminated in time & space (UMN lesions) Myaesthenia Gravis - autoimmune disorder characterised by muscle weakness & fatiguability, antibodies against AChR (LMN lesions) Motor Neurone Disease or ALS - progressive selective loss/degeneration of neurones in the upper & lower motor tracts, sensory neurones are spared, eye movements never affected (LMN AND UMN)
73
Weber's & Rinne's Test Interpretation
WEBER'S - normal = equal - sensioneural loss = louder in 'good ear' - conductive loss = louder in bad ear RINNE'S - normal = AC > BC - sensioneural = AC > BC due to both air and bone conduction being reduced equally - conductive hearing loss = BC > AC