Neurology Flashcards
indications for a lumbar puncture
Diagnosis of meningitis/encephalitis
Diagnosis of SAH - If clinically suspected but no abnormalities on CT
Measurement of CSF pressure (Idiopathic intracranial hypertension)
Therapeutic removal of CSF (Idiopathic intracranial hypertension)
Intrathecal drug administration
Diagnosis of miscellaneous conditions (behcets, MS, neurosyphillis)
where do you do an LP
L4/L5 space
csf finding in MS
Moderately raised protein levels - <1g/L
Up to 50 lymphocytes/mm3
Oligoclonal IgG bands on electrophoresis
complications of LP
Post LP headache
Occurs in 30%, onset within 24 hours with resolution over 2 weeks
Classically a constant bilateral dull ache
Worse when upright, as due to intracranial hypertension
Treat with analgesics +/- blood patch (Re-injection of a patients own blood to form a clot)
Dry-tap
Usually due to poor technique
Infection
Damage to spinal nerves
Causes weakness/paresthesia
Coning of cerebellar tonsils
contraindications for LP
Suspicion of mass in the brain/spinal cord/raised ICP
This can lead to coning of the cerebellar tonsils
Any unconscious patient must have a CT prior to LP
Overlying/local infection
Congenital lesions in the area
Meningomyelocele
Problems with haemostasis
Platelets <40
Clotting abnormalities
Anticoagulation
Haemodynamic instability
what does xanthochromia in the CSF indicate
bleeding in the brain
contraindications for an MRI
Electrically, magnetically or mechanically activated implants
Pacemakers, cochlear implants, drug infusion pumps
Implants containing ferrous material
Aneurysm clips
Surgical staples
Bullets, shrapnel, metal
Screen patients with XR if they have a history of metal foreign bodies in the eye
Some implants are now MRI safe
acute management of a head injury
Ensure C-spine is secured
A-E resus
A: some level of intubation usually required
Record GCS prior to intubation
B: chest injuries often co-exist and lead to an additional secondary brian injury from hypoxia
C: shock occurs in polytrauma patients – ensure cross match is done ASAP
Record GCS
Brief history if conscious
Neurological exam
Check for signs of deterioration
Most important - Changing pupillary responsiveness
As ICP rises there is initially a progressive dilation on the side of the lesion, with sluggish response to light
If bilateral it is a pre-terminal sign
Falling pulse/rising BP
Cushings reflex: late sign
Manage appropriately if signs of rising ICP
Appropriate imaging
CT head if indicated
C spine radiography if indicated
Always indiated if there is a TBI with LOC
Prevent secondary insults
Hypoxia
Hypercapnia leads to cerebral vasodilation –
increasing cerebral blood volume and raising ICP
Raied ICP patients may be hyperventilated in ICU
Hypoxaemia also leads to cerebral vasodilation, as well as causing profuse lactic acidosis which damaged cerebral neurones – not breathing for 4 minutes starts to cause irreversible brain damage
Hypovolaemia
MABP between 60-160 mmHg is autoregulated
Following a head injury this autoregulation goes and therefore cerebral perfusion relies on SBP
As such , this resus is vital to regulate SBP and therefore brain perfusion
Hypoglycaemia
GCS 15 and haemodynamically stable = patients can be discharged
Period of unconciousness after a head trauma = head Xr required before discharge
Discharge with a head injury warning card
If intoxicated they need to be admitted as its hard to differentiate between intoxication and brain injury
indications for CT head within 1 hour during a head injury
GCS <13 at the time, or <15 2 hours after the injury
Focal neurological deficit
Signs of increasing ICP: Headache Blurred vision Vomiting Decreased awakeness Seizure Weakness Anergy
Suspected skull #
Post-traumatic seizure
Vomiting >1 times
indications for a CT head within 8 hours after a head injury
Anticoagulated patients
LOC + >65/Dangerous mechanism of injury (fall from a height)/Retrograde amnesia >30 mins/Inability to recall events before injury
when should you admit a patient following a TBI
If imaging show pathology
If GCS <15
If this is the case monitor them every 30 minutes
Continuous worrying signs
Tx status epilepticus
A-E
100% oxygen
Oral/nasal airway
IV access
Bloods Glucose Calcium Magnesium FBC U+E LFT clotting
CXR to rule out aspiration
Take urine sample if possible
ABG
Set up ECG
if >5 mins
IV lorazepam
4mg bolus repeated after 5 mins if no response
Finger prick glucose
If hypoglycaemia 50ml 50% glucose IV
Any suspicion of alcoholism
IV pabrinex – 2 ampoules over 10 mins
In females of childbearing age do a pregnancy test
If seizure activity persists despite 8mg of lorazepam
IV phenytoin 15mg/kg slow infusion (50mg/min)with ECG monitoring
EEG monitoring useful if unsure about nature of status
> 10 mins = call ICU
They may intubate under thiopentone (GA)
Tx neuromuscular ventilatory compromise
CALL FOR HELP – CRIT CARE
Ensure airway is safe
Sit up, O2 monitoring, HR and saturations (90-92)
Suctioning If secretions
NBM
Blood gases
IV access
CXR for ?infection
Further investigation for critical care and neurology
characteristic finding on CT with extradural haematoma
lentiform lesion
midline shift
ventricle compression
Tx extradural haematoma
Urgent neurosurgical referral
Burr hole to release pressure
Prognosis very good if this is performed early
Very minor it may be managed conservatively with regular monitoring
in base of the skull fractures what are given if there is a csf leakage
prophylactic antibiotics
Tx for base of skull fractures
urgent neurosurgical referral
Tx for acute hydrocephalus
Only definitive management is surgery so medical management exists to delay that
Azetazolamide +/- furosemide
Azetazolamide is a carbonic anhydrase inhibitor and is usually used in glaucoma to prevent the production of intraocular fluid, but in this case it reduces the amount of CSF produced
Surgical management
Ventriculoatrial, or ventriculo-peritoneal shunting for progressive symptoms
Valves open at certain pressures to allow release of CSF
Neurosurgical removal of tumours if necessary
Endoscopic 3rd ventriculostomy is an alternative procedure for obstructive hydrocephalus
Hole is made in 3rd ventricle so the CSF can bypass the cerebeal aquaduct (most common site of malformation) and drain into the interpeduncular cistern
GCS components
Motor
1 – no response
2 – extensor response to pain
3 – flexor response to pain
4 – withdraws from pain, pulls limb away
5 – localises to pain, responds towards painful stimuli
6 - Obeys commands
Voice
1 – no speech
2 – incomprehensible muffled speech
3 – inappropriate speech, understandable but no conversational effort
4 – confused orientation, answers questions with some confusion
5 – oriented
Eyes
1 – no eye opening
2 – eyes open in response to pain
3 – eyes opening in response to speech
4 – eyes open spontaneously
how is GCS score roughly stratified
13-15 = mild injury
9-12 = moderate injury
<9 = severe injury
what is cheyne-stokes breathing and what does it indicate
rapid breathing following by apnoea
coning
what does a unilaterally enlarged pupil indicate in the context of a semi concious patient
raised ICP
what does a bilaterally enlarged fixed pupil indicate in the context of a semi-concious patient
Deep coma
Brainstem death
what does a bilateral pinprick indicate in the context of a semi-concious patient
opiate overdose
pontine lesions causing sympathetic interruption
what are some important points in the history of a ?stroke
Exact time of onset
Speed of symptom onset
Body parts affected
Seizure?
Previous history of stroke?
Diabetic?
Tumours?
AF/MI?
On anticoagulants?
Drugs/smoking/alcohol?
how should you examine a ?stroke patient
GCS
NHISS
National institute of health stroke scale
Combines several parts of a clerking exam into a single scale evaluating possible location, thrombolysis benefit and severity stratification
CVS Murmurs (endocarditis) Signs of dissection BP HR
Respiratory
SpO2
RR
Crackles?
Neuro
LMN/UMN
CNS
Cerebellar
indications for urgent (<1 hour) brain CT in ?stroke
If considering thrombolysis
If bleeding risk
If decreased consciousness
Neck stiffness
Tx of confirmed embolic stroke
A-E management
Withold antiplatelet therapy until haemorrhage excluded
If ischaemic stroke confirmed administer 300mg aspirin
If <4.5 hours including at least 30 minutes of symptoms start thrombolysis
Thrombolysis
First check for contraindications (see table below)
Must have lab results back (clotting + platelets)
0.9mg/kg alteplase as per clinical pathway in hospital
10% bolus over 1 minute, remainder over 60minutes
post thrombolysis Tx for strokes
SALT
Swallow assessment within 2 hours – also helps with communication
Physiotherapy Relieves spasticity Prevents contractures Baclofen may be used to relieve spasticity Early mobilisation is vital
Occupational therapy
Limb splinting, ward groups
Nursing Implement SSKIN bundle Early nutrition required if NBM LMWH anticoagulation started on day 3 post-ischaemic stroke Ensure TED stockings are being worn
post thrombolysis Tx for strokes
SALT
Swallow assessment within 2 hours – also helps with communication
Physiotherapy Relieves spasticity Prevents contractures Baclofen may be used to relieve spasticity Early mobilisation is vital
Occupational therapy
Limb splinting, ward groups
Nursing Implement SSKIN bundle Early nutrition required if NBM LMWH anticoagulation started on day 3 post-ischaemic stroke Ensure TED stockings are being worn
post discharge stroke management
Lifestyle Cardioprotective diet Stop smoking Reduce drinking Exercise more
Antihypertensive therapy
Most importantly
Start 2 weeks post stroke if there is elevated BP
BP should be lowered slowly as autoregulation is likely impaired
Antiplatelet therapy
Aspirin 300mg daily for 2 weeks
Clopidogrel 75mg therafter
Statin
Offer 48 hours post stroke independent of cholesterol levels
Manage comorbidities
Strict diabetes management
Control AF well
Carotid USS will also be undertaken
post-stroke complications
Malignant MCA syndrome (Rapid neurological deterioration due to cerebral oedema associated with MCA infarcts)
DVT/PE
Aspiration + hydrostatic pneumonia
Pressure sores
Depression
Seizures
Incontinence
Post-stroke pain
Worsens outcomes
Multifactorial in nature
Often requires pain team input
Tx of Malignant MCA syndrome
NICE recommends empirical treatment in any patient <60 with a CT/MRI showing an infarct of at least 50% in the MCA with decreasing GCS
Treatment = rapid decompressive hemicraniectomy
what factors make a patient ‘high risk’ for stroke post TIA
TIA when anticoagulated
Multiple TIAs (especially in a short period of time)
ABCDD score >3
Age
>60 is 1 point
Blood Pressure
>140/90 = 1 point
Clinical features
Unilateral weakness = 2 points
Speech disturbance without weakness = 1 point
Duration of symptoms
>60 mins = 2 points
10-59 minutes = 1 point
Diabetes
1 point
Tx for patients that have had a TIA and have been determined high risk for stroke
Statin
300mg aspirin
Unless currently taking low dose aspirin
Arrange referral to a specialist clinic in 24 hours
Advice patients not to drive until seen by specialist
Tx for patients that have had a TIA and have been determined low risk for stroke
Statin
300mg aspirin
Unless currently taking low dose aspirin
Arrange referral to a specialist clinic within a week
Advice patients not to drive until seen by specialist
what is required to diagnose a venous sinus thrombosis
MRI angiography
Tx of haemorrhagic stroke
Antiplatelets/anticoagulation CONTRAINDICATED
Reverse anticoagulation
Lower BP to <140/90 in 1 hour
IV labetolol
Neurosurgical intervention may be required
If GCS is falling and there is evidence of coning
complications of subarachnoid haemorrhage
Death
30% die immediately
Rebleed
Aneurysms - Inital bleed may be fatal but with sufficient vasospasm a clot may form
This usually holds for 3-4 days before rebleeding
AVMs
Generally rebleed within a few years rather than days
Hydrocephalus
Due to fibrosis of CSF pathways from the insult
Cerebral vasospams
May be severe leading to delayed vascular damage
investigation of ?SAH
Bloods FBC U+E LFT ESR Clotting G+S
CT Initial investigation of choice Usually seen within 48 hours Quantity of blood should be estimated for prognosis AVM usually visible on CT
LP - if CT normal
Should be done >12 hours after symptom onset
CSF will become xanthochromic (yellow from bilirubin) – visual inspection is sufficient for diagnosis
CT/MRI Angio - for surgery
Tx for SAH
4 weeks bed rest
Hypertension control
Nimodipene – reduces vasospasm, reduces mortality
Give to all if BP allows
IV fluids – may also prevent further vasospasm
Analgesia, anti emetics
Stool-softners to prevent straining
Discuss with neurosurgery
10-20% will rebleed within a few weeks
Aneurysms will usually be coiled by interventional radiology due to imminent risk of rebleed
Some will require neurosurgical clipping
AVMs usually rebleed within years rather than days but are generally dealt with at the time of presentation
Coiling by IR more common but gamma knife therapy may also be done
11% of patients develop hydrocephalus and require a shunt
what is the sign of an acute subdural hematoma on CT head
crescent shape pool of blood with midline shift and ventricle occlusion
management of acute subdural haematoma
craniotomy
what are the signs of a chronic subdural hematoma on CT head
blood becomes dark and assumed a more lentiform shape (like extradural)
Tx tension headache
If episodic (<15d/month) Paracetamol Aspirin NSAIDS Advice not to overuse the medication
If medication is used more than twice a week consider preventative treatment
Low dose amitryptaline
75mg initally, titrated upwards if there is a partial response
Chronic tension headache is more difficult to treat
Reassurance, relaxation techniques and addressing underlying stressors are important
Medication overuse headaches and clinical depression should be excluded and/or treated
Tx cluster headaches
Exclude secondary causes and other causes of eye pain
e.g. acute angle closure glaucoma
Subcutaneous triptan to take at the start of an attack
Home oxygen for use during the attack
At least 12/L min through non rebreathe
Not for COPD
Oral triptans/oral analgesia not effective for the acute attack
Prophylactic treatment is with alcohol avoidance and verapamil (off-license)
Tx Migraines
Examine to rule out other differentials Signs of focal neurology Raised ICP Meningism Temporal arteritis Retinal haemorrhage (SAH)
Headache diary Frequency Severity of attacks Precipitants Exacerbating/relieving factors Avoidance of external triggers
In the acute attack
First line is an oral NSAID or paracetamol + anti emetic (metclopramide)
2nd line is a triptan (oral, sumutriptan) taken as soon as possible on the onset of symptoms
Can be intranasal if vomiting prevents oral treatment
Opioids should not be used
Follow up, as repeated unsuccessful triptan treatment therapy is rare (10%) if the underlying diagnosis is actually migraines
Preventative treatment
Consider if migraine attacks are causing significant disability
>2 a month
Topiramate or propanolol are first line
Propanolol in women of child bearing age
Amitryptiline/anticonvulsants if these arent successful/ tolerated
what patient population should you avoid triptans in
Avoid if IHD, uncontrolled HTN, coronary artery spasm
why is the COCP avoided in women that have migraines
Slight increase in stroke risk in those on COCP greater if migraine sufferers
Tx menstrual related migraine
mefanamic acid from the first day or menses throughout menstruation, or triptans 2 days before the expected time of period
presentation of idiopathic intracranial hypertension
visual disturbance + headaches in a younger obese woman
may be a pulsatile tinnitus and a 6th nerve palsy
Tx idiopathic intracranial hypertension
weight loss generally causes spontaneous remission
definitive management is a surgical shunt
trial of corticosteroids may also be successful
Tx trigeminal neuralgia
Simple analgesics are ineffective, with carbamazepine offering good symptom control
Tx atypical face pain
anti-depressants (if patient has depression/anxiety)
Tx newly diagnosed brain cancer
Dexamethasone 5-6mg QDS
If any neurological deteriation or drowsiness
Anticonvulsants
If presented with epilepsy
Refer to neuro-oncology MDT
Neurosurgical intervention if accessible, often with adjunctive therapy
give examples of paraneoplastic syndromes
Myasthenia gravis
Lambert-eaton myasthenic syndrome
Paraneoplastic sensory neuropathy
Paraneoplastic cerebellar degeneration
signs of paraneplastic cerebellar degeneration
Gives classical cerebellar signs
Ataxic gait
Dizziness
Dysarthria
what cancers typically cause paraneoplastic cerebellar degeneration
Frequently associated with hodgkin lymphoma, breast cancer, small cell lung cancer and ovarian cancer
what is the triad of normal pressure hydrocephalus
Dementia - (wacky)
Urinary incontinence (wet)
Apraxic gait (wide, shuffling, short gait with difficulty beginning and turning whilst walking) - (wobbly)
Tx for normal pressure hydrocephalus
Some patients respond to ventriculoperitoneal shunting
Only indicated if they respond to trials of lumbar drainage
what does an indian ink stain test for whilst investigating CSF
fungi
Empirical treatment of ?meningitis in a non-blanching rash
- 2g IM benzylpenicillin STAT
- 4mg 4 hourly following this
cefotaxime can then be used in the tx of penicillin allergic patients
Tx of confirmed bacterial meningitis
If <60 and not immunocompromised
IV ceftriaxone 2g BD
Cloramphenicol used in pen allergic patients (25mg/kg IV)
IV dexamethasone
2 doses 6 hours apart given with first Abx dose
> 60 or immunosuppressed (this includes diabetes)
IV ceftriaxone 2gBD
IV amoxicillin 2g 4 hourly
IV dexamethasone
Tx of herpes encephalitis
IV aciclovir for 10 days
what Abx is used as a prophylactic dose for close contacts in a confirmed case of meningococcal disease
Ciprofloxacin
acute complications of meningitis
Sepsis/DIC
Hydrocephalus
Adrenal haemorrhage: waterhouse-friedeerichsen syndrome
chronic complications of meningitis
Seizures
Brain abscesses (Generally very rare)
Cranial nerve palsies
Ataxia/muscle hypotonia
Tx brain abscess
Tx = surgical drainage, broad spectrum Abx and high dose corticosteroids
what organism is most likely to cause an acute spinal abscess
staph aureus
Tx for acute spinal abscess
emergency imaging, ABx and decompression
what type of herpes zoster virus causes encephalitis over meningitis
HSV-1 (HSV-2 causes meningitis most commonly)
prognosis of viral encephalitis
mortality is 20%
what is Todd’s paralysis
temporary paralysis of the limb post partial seizure
what are features of temporal lobe epilepsy
Classic aura with a sense of fear/deja-vu and hallucinations
Confusion/anxiety and automatisms
Lip smacking
Chewing
what stimulates absence seizures
hyperventilation or glashing lights
Tx Generalised seizures
1st line is valproate or lamotrigine in females of childbearing age
Adjuncts may be clozabam, carbamazepine or levetiracetam
Tx absent seizures
Ethosuximide
Tx partial seizures
Carbamazepine or lamotrigine in females of childbearing age
Multiple adjuncts used
side effects of sodium valproate
rash, sedation, weight gain, hair loss or tremor
Also associated with birth defects, thrombocytopenia, increased risk of pancreatitis and liver damage
main risk of lamotrigine
bone marrow suppression
main risk of carbamazepine
agranulocytosis
side effects of phenytoin
Gum overgrowth
Nyastagmus
what are some overall principles to stick by when treating epilepsy
All can cause leucopenia, rashes, SJS, TEN
Refractory cases require adherence and alcohol/drug use checking, as well as considering a SOL
Withdrawal may be allowed is the patient is seizure free for 2-4 years and the drug should be reduced in dose every 4 weeks with the patient stopping driving during withdrawal
what are the driving laws surrounding epilepsy
If a patient has had a seizure they should inform the DVLA and stop driving immediately
If the attack was whilst they were awake and there was LOC their license is revoked
Patients may apply again if they are seizure-free for 6 months after 1 seizure, 1 year after multiple seizures
Patients with sleep-related epilepsy can drive If the past 3 years have had only sleep-related seizures
what are the rules around treating epilepsy and pregnancy
Majority of epilepsy drugs are associated with neural tube defects
It still must be treated in pregnancy as risk of neural tube defects is still preferable to hypoxic seizures
Lamotrigine is first line in women of childbearing age
Any woman with epilepsy that is pregnant should be taking 5mg folic acid during the first trimester and should be seen by a consultant throughout the pregnancy
They should also have vitamin K in the 3rd trimester due to risk of foetal bleeding
What tests are most helpful to diagnose MS
MRI - gold standard
CSF - oligoclonal bands on electrophoresis in 80%
Visual evoked responses (95%)
management of acute MS attack
Investigate any cause
Infection
Consider admission if the relapse is severe or the patient cannot meet their social care needs at home
High dose corticosteroids
Oral methylprednisolone 0.5g/day for 5 days
May reduce severity of attack but no effect on long term course of disease
Start as soon as possible
Assess any increase in social care
Patient education
Steroids help symptoms but may cause confusion/depression
Significant recovery expected within 2-3 months there may be residual symptoms
General management of MS
Should be under a specialised MDT
Lifestyle
Stop smoking
Exercise
Prompt recognition and treatment of co-existing infections
UTIs in particular are a bit exacerbator
Assess for and treat complications
Offer disease modifying therapy
Interferon beta and glamatier no longer reccomended by NICE
Relapsing remitting
Demethyl fumarate/teriflunomide
Natalizumab for severe MS (2 or more disabling relapses in a year)
Decreases relapses by 2/3
complications of MS
Fatigue
Spasticity
Constipation/pressure sores
Ataxia/tremor
Depression
Urianation
Sexual dysfunction
Tx for complications of MS
Fatigue
Poorly understood
Cognitive approaches and amantidine may be helpful
Spasticity
Baclofen and physiotherapy is first line
Consider factors affecting spasticity
Dantrolene/botox injections for refractory spasticity
Ataxia/tremor
No pharmacological treatment recommended
Physiotherapy/OT referral should be considered
Mobility issues
Aids if required
Aim for physio or vestibular rehabilitation
Depression
CBT
Marked depression is common
Urination
Post void bladder scan <100ml = training/oxycontin/tolteradine
Post void bladder scan >100ml = teach intermittent catheterisation
Sexual dysfunction
Siladefenil for men
Pressure sores
Encourage movement/physio and regular checking for
sores
Prognosis of MS
Average life expectancy from diagnosis is 20-30 years
May be a long latent episode (15-30 years) from an episode of optic neuritis before further symptoms occur
Prognosis is better if there is a sensory onset
poor prognostic features of MS
Increase age of presentation
Early cerebellar involvement
Loss of mental functions
Causes of cerebellar dysfunction
MS Alcohol Vascular disease Iatrogenic/infective/inherited (freidrich's ataxia) SOL
Tx parkinsons
Specialist MDT
Social care important
Levodopa + COPA Decarboxylase
to delay L-Dopa therapy (as there is a wearing off effect) these drugs may be used:
Dopamine agonists (bromocriptine/cabergoline/ropinarole)
MAOIs (selegine)
COMT-is (entacapone)
side effects of levodopa
Nausea
Vomiting
Confusion
Visual hallucinations
Chorea
what anti-emetic can be used for parkinsons disease
domperidone
what are ergot derivatives (bromocriptine/cabergoline) associated with and what should be done about it
pericardial/pulmonary/retroperitoneal fibrosis
should be monitored via Echos, pulmonary function tests and ESR
surgical options for parkinsons
Deep brain stimulation
Thalotomy
prognosis parkinsons
Progressive disease and most patients will succumb to complications within 10 years
Tx Dementia
MDT
Social care very important
Carer assessment
Occupational therapy functional and home assessment
Reduce vascular risks BP Lipid profile Glycaemic control Particularly in VD – but do for all
Cognitive stimulation therapy
Group classes
May slow decline
Mild-moderate AD/LBD ACh inhibitors (Donepezil/Galantamine/Rivastigmine)
Severe NMDA receptors (Memantin) ]
Manage the behavioural and psychological symptoms of dementia (BPSD)
Non-pharmalogical as much as possible
Antipsychotics increase risk of stroke and therefore should only be prescribed by a specialist
symptomatic control of delirium
1 to 1 nursing
Hydration
Promote orientation
Control pain but avoid any sedative drugs
management of motor neurone disease
Specialist MDT management
Social and carer assessment important
Disease-modifying therapy
Riluzole
Increases presynaptic glutamate
increases survival in ALS patients by an average of 3-4 months
Nutritional support
From an early stage, it can produce increases in QOL
Gastrostomy tubes may be placed late in the disease if the swallowing function is lost
Respiratory support
NIPPV considered if respiratory weakness is still an issue
prognosis of motor neurone disease
Remission from MND is not known
Death is eventually from bronchopneumonia or respiratory failure from weakness of respiratory muscles
4 most common causes for peripheral neuropathy
Diabetes
Carcinomatous
B vitamin deficiency
Drugs
management of guillan barre syndrome
Severe cases progress rapidly over hours-days
Nurse on high dependency units
Pay attention to pressure sores, chest infections and DVTs
Cases involving respiratory muscles require intubation
FVC should be regularly monitored
SC heparin + pressure sores reduce risk of DVT
If presenting within the first 2 weeks, high dose IV immunoglobins will reduce the severity and duration of paralysis
Corticosteroids have no therapeutic benefit
prognosis of guillan barre syndrome
In mild cases there is little disability before spontaneous recovery
Complete recovery occurs over months – 80-90% recover completely
Some left with residual weakness
Tx of shingles
5-7 days oral acyclovir
Paracetamol/amitryptaline for pain
what is a sensitive indicator for opthalmic herpes and why Is it important to recognise
opthalmic herpes may lead to May lead to
Uveitis, Corneal scarring, Secondary panopthalmitis and is potentially light threatening
Heralded by shingles on the tip of the nose – most sensitive factor
This is called hutchinsons sign
post-herpetic neuralgia Tx
like any neuropathic pain amitrypatline and topical capsaicin for example
Tx myathenia gravis
Avoidance of certain Abx that induce NM blockade
Aminoglycosides
(Gentamicin, Neomycin, Vancomycin)
Lifelong long-acting oral ACh-esterase
Neostigmine, Pyridostigmine
Corticosteroids for relapses
Starting in hospital as increasing weakness early on
Simultaneous identification + treatment of the trigger
Weakness of respiratory muscles can be life-threatening
Monitor FVC
May need a ventilator
Severe cases need IVIg/plasmaphoresis
Alternate-day regimen at discharge
Steroid sparing agent is azathioprine
Thymemectomy
Performed at any age increases chance of remission
prognosis opthalmoplgeia
MG may never progress beyond opthalmoplgeia and periods of remission for up to 3 years may occur
Outlook is poor if there is respiratory muscle involvement
most common musclular dystrophy
duchennes
management of a patient with an impaired motor function
Manage as per the REPAIR mnemonic
Spasticity
Physical management - Physio, Gait training
Removal of exacerbating stimuli
Surgical management
Tendon lengthening
Releases for fixed deformities
Electrostimulation therapy
Medical management Baclofen Dantrolene Benzodiazepines Botulinum Toxin injection
Contractures
Aim to prevent development
