Neuro Flashcards
Red flags for headaches:
- Thunderclap
- Refractory pain
- Progressive or persistent daily headache
- Papilloedema
- Features of raised ICP
- Visual loss
- Scalp tenderness
- Atypical aura or duration
- Progressive neurological deficit
- Unexplained cognitive or behavioural change
- Cancer history or immunosuppression
Acute change in cognition and behaviour with headache:
Encephalitis
Scalp tenderness with headache think…
GCA / Temporal arteritis.
Indications that a patient is suffering from a medication overuse headache.
- Headache occurs 15 days or more per month and
- Has been using regular acute / symptomatic headache medication for 3
- months (“regular” = 10+ days per month of ergotamines, triptans, opoids OR
- 15+ days per month of simple paracetamol or NSAIDs) and
- No other headache diagnosis more appropriate
What class of medication is topiramate?
- When is it used?
- Contraindications?
Anti-epileptic
- Used for migraine
- Contraindicated in pregnancy
Note: Also causes weight gain.
What are Monoamine oxidase inhibitors and COMT inhibitor used for what and how do they work?
Used to treat parkinson’s by preventing the breakdown of dopamine.
Common side effects of Ldopa:
- Hypotension
- Restlessness
- Gastrointestinal upset
- In rare cases, dopamine excess can result in psychiatric reactions including acute psychosis.
Summarise the classic presentation of a cluster headache:
This is the classic presentation of cluster headaches. They tend to present as unilateral peri-orbital headaches and are associated with ipsilateral ptosis, lacrimation, conjunctival injection and rhinorrhea. They classically occur in clusters over a few weeks, with a “silent” period in between them in which the patient does not experience headaches
A 65-year-old lady presents to her GP with a new-onset left-sided lower motor neuron facial palsy and mild-to-moderate left-sided otalgia. She suffers from hypertension and diverticular disease. On examination there is a tender vesicular rash found inside the external auditory canal on the left-side; the right side is normal. Hearing appears normal for her age.
What is the most likely diagnosis?
Ramsay Hunt Syndrome type II
This is the correct answer. Ramsay Hunt syndrome type II is a reactivation of varicella zoster virus in the geniculate ganglion. It causes a unilateral acute facial nerve paralysis in addition to an erythematous vesicular rash in the ear canal. Occasionally otalgia precedes the rash and facial palsy.
Negative findings on CT for someone with a thunderclap headache… what’s next?
- what are you looking for?
LP looking for presence of RBC’s and xanthocromia.
What is xanthochromia?
Xanthochromia is the presence of bilirubin in the cerebrospinal fluid and is sometimes the only sign of an acute subarachnoid hemorrhage
Extradural haematoma is classically due to injury to what artery?
Classically due to injury of the middle meningeal artery, a branch of the maxillary artery (from the ECA).
EDH vs SDH findings on CT
EDH = lemon shaped does not cross sutures.
SDH = Cresecent shaped, does cross sutures.
What is the most common primary brain tumour?
Glioblastoma multiforme
Summarise meningiomas:
Meningiomas are typically benign, extrinsic tumours of the central nervous system. They arise from the arachnoid cap cells of the meninges and are typically located next to the dura and cause symptoms by compression rather than invasion.
What is the most common primary brain tumour in children.
Pilocytic astrocytoma
Treatment for pituitary adenoma:
Treatment can either be hormonal or surgical (e.g. transphenoidal resection).
What hereditary syndromes cause brain tumours?
Neurofibromatosis
Tuberous sclerosis
How glioblastoma’s appear on CT/MRI imaging?
On imaging they are solid tumours with central necrosis and a rim that enhances with contrast. Disruption of the blood-brain barrier and therefore are associated with vasogenic oedema.
Where are meningiomas typically located?
They typically are located at the falx cerebri, superior sagittal sinus, convexity or skull base.
Often stuck on the outside.
Tumours that commonly metastasise to the brain:
lung (most common)
breast
bowel
skin (namely melanoma)
kidney
1p 19q deletion = what cancer?
Oligodendroglioma
1DH1 mutation = what brain tumour?
Astrocytoma
MGMT promoter methylation is seen in what brain tumour?
Glioblastoma
What is the issue with benign brain tumours?
- Grow by expansion, compressing surrounding structures.
- Some invade surrounding brain / blood vessels / tissues
- Can be difficult to get to, and / or remove.
Most common primary source of secondary brain mets?
Lung cancer (SCC)
Most common location in the brain for brain mets?
Cerebrum 80%
Cerebellum 15%
Brain stem 5%
What are the two main drugs used in the management of brain cancer?
Dexamethasone
Anti-epileptics
Best imaging for brain tumours?
MRI!
- Shows the anatomy better.
- Functional MRI looking at primary cortical areas.
Rule of thirds for brain mets:
1/3 = 1 met
1/3 = <4 mets
1/3 >4mets :(
How to decide who to treat with brain mets?
Only aim to treat patients with less than 4 brain mets.
Need to assess performance score.
When to biopsy for brain cancer?
When surgery / resection isn’t possible.
When are awake surgeries helpful?
When the tumours are located in the speech areas of the brain.
Chemotherapy drugs used for brain cancers:
Temozolamide
PCV (Procarbazine, CCNU, Vincristine)
Lomustine alone
Other
* Avastin - controls oedema around the tumour.
* Tamoxafen
Mainstay of treating brain cancers:
Radiotherapy!
Note: Radiosurgery is sometimes used for patients to give a focused dose to small lesions (mets/meningiomas).
Clinical features of encephalitis:
ALTERED MENTAL STATUS
Other suggestive features include fever, a flu-like prodromal illness, and early seizures.
What is the most common cause of encephalitis?
HSV-1
- responsible for 95% of cases in adults.
This said HSV-2, cytomegalovirus, epstein barr virus, varicella-zoster virus, HIV and the arboviruses (including west nile virus) can also cause a similar picture.
Where in the brain is typically affected in encephalitis?
Temporal and inferior frontal lobes
What investigations should be carried out for encephalitis?
LP - CSF shows:
Lymphocytosis
Elevated protein
PCR for HSV, VZV and enteroviruses.
Neuroimaging - MRI
Medial temporal and inferior frontal changes (e.g. petechial haemorrhages)
normal in one-third of patients.
Treatment for encephalitis:
Aciclovir
Ceftriaxone
Treatment of encephalitis including doses:
2g IV ceftriaxone BD
10 mg/kg aciclovir TDS for two weeks.
What is meant by encephalopathy?
Clinical syndrome of altered mental status; manifesting as reduced consciousness or altered cognition, personality or behaviour.
Has many causes including systemic infection, metabolic derangement, inherited metabolic
encephalopathies, toxins, hypoxia, trauma, vasculitis, or central nervous system infection.
What is meant by encephalitis??
Inflammation of the brain
Strictly a pathological diagnosis; but surrogate clinical markers often used, including CSF
inflammatory change or changes on neuroimaging
Causes include viruses, small intracellular bacteria that directly infect the brain
parenchyma and some parasites
Can also occur without direct brain infection, for example in acute disseminated
encephalitis myelitis (ADEM), or antibody-associated encephalitis.
What is Cushing’s triad?
Bradycardia, irregular respiration, wide pulse pressure.
The triad represents raised ICP.
When to delay lumbar puncture in encephalitis?
Get imaging first in GCS less than 14.
Bleeding disorders.
Immunocompromised.
Signs of raised ICP - papilloedema, cushing’s triad.
Focal neurological signs, recent onset seizures.
CSF findings in encephalitis:
CSF is gin clear
Slightly increased cells 5-1000, predominantly leucocytes
Normal CSF / Plasma glucose ratio
CSF findings in bacterial meningitis:
CSF cloudy.
High cell count (neutrophils).
High protein.
What is seen on an MRI for MS patients?
Typically periventricular white matter lesions are seen on MRI.
Acute managment of MS:
Methylprednisolone
Must rule out infection first
How are the treatment for chronic MS divided?
Disease modifying drugs
Symptomatic therapies
What disease modifying drugs are used to manage MS?
- First-line injectables such as beta-interferon and glatiramer
- New oral agents such as dimethyl fumarate, teriflunomide and fingolimod
- Biologics such as natalizumab and alemtuzumab.
Symptomatic therapies for chronic MS:
- Physiotherapy
- Baclofen and BoTox for spasticity
- Modafinil and exercise therapy for fatigue
- Anticholinergics for bladder dysfunction
- SSRIs for depression
- Sildenafil for erectile dysfunction
- Clonazepam for tremor
Clinical features of essential tremor:
- postural tremor: worse if arms outstretched
- improved by alcohol and rest
- most common cause of titubation (head tremor)
Management of essential tremor:
Propanolol
Behavioural techniques and physical therapy
Parkinson’s triad:
Asymmetric tremor, rigidity and bradykinesia
Features of a cerebellar tremor:
including examination
Intention tremor
Cerebellar signs e.g. Past-pointing, nystagmus etc
Mnemonic to remember features of cerebellar dysfunction:
DANISH
- Dysdiadochokinesia (an inability to perform rapid alternating hand movements)
- Ataxia (a broad-based, unsteady gait)
- Nystagmus (involuntary eye movements)
- Intention tremor (seen when the patient is asked to perform the ‘finger-nose test’)
- Slurred speech
- Hypotonia
Causes of cerebellar dysfunction:
Vitamin C
The differentials of cerebellar dysfunction can be remembered by going through a surgical sieve (remembered by the mnemonic: VITAMIN C):
- Vascular causes include stroke(ischaemic or haemorrhagic affecting the posterior circulation).
- Infective causes include Lyme disease.
- Inflammatory causes include multiple sclerosis.
- Traumatic causes include trauma to the posterior fossa.
- Metabolic causes include alcoholism.
- Iatrogenic causes include drugs such as phenytoin and carbamazepine.
- Neoplastic causes include primary tumours (e.g. cerebellopontine angle tumour, acoustic neuroma) and secondary tumours (metastases e.g. breast cancer, lung cancer).
- Congenital/hereditary causes include Friedrich’s ataxia, and the spinocerebellar ataxias.
Most common cause of cerebellar dysfunction:
Stroke
MS
What are the different causes tremor?
Essential tremor
Cerebellar dysfunction (intention tremor
Idiopathic (PD) (resting rolling pill tremor)
Explain the clinical features of Brown-Sequard syndrome:
Disruption of descending lateral corticospinal tracts, ascending dorsal column and ascending spinothalamic tracts leads to the following findings below the level of the injury:
- Ipsilateral hemiplegia
- Ipsilateral loss of proprioception and vibration
- Contralateral loss of pain and temperature sensation
Common causes of Brown-Sequard syndrome:
Common causes of BSS include:
- Cord trauma (penetrating injuries being the most common)
- Neoplasms
- Disk herniation
- Demyelination
- Infective/ inflammatory lesions
- Epidural hematomas
Explain the management of Brown-Sequard syndrome:
Management of BSS depends on the causative pathology. Need for conservative or surgical management depends on patient’s neurological status and clinico-radiological findings. Surgery intervention is advised in post-traumatic BSS if there is presence of retained foreign objects, CSF leakage, infection or signs of extrinsic spinal cord compression.
Medical management is preferred for infective/ inflammatory or demyelinating causes of BSS while surgical treatment is performed for pathologies causing extrinsic cord compression.
Important investigations for epilepsy:
An electroencephalogram(EEG) can showtypical patterns in different forms of epilepsy and support the diagnosis.
An MRI brain can be used to visualise the structure of the brain. It is used to diagnose structural problems that may be associated with seizures and other pathology such as tumours.
Other investigations can be used to exclude other pathology, particularly an ECG to exclude problems in the heart.
What is meant by ‘tonic clonic’
Tonic = muscle tensing
Clonic = muscle jerking
First and second line management of tonic clonic seizures:
- First line: sodium valproate + Levetiracetam
- Second line: lamotrigine or carbamazepine
Where do focal seizures start and what do they effect?
Focal seizures start in the temporal lobes. They affect hearing, speech, memory and emotions.
How can focal seizures present?
- Hallucinations
- Memory flashbacks
- Déjà vu
- Doing strange things on autopilot
Treatment of focal seizures:
One way to remember the treatment is that they are the reverse of tonic-clonic seizures:
- First line: carbamazepine or lamotrigine
- Second line: sodium valproate or levetiracetam
Summarise absence seizures:
Absence seizures typically happen in children. The patient becomes blank, stares into space and then abruptly returns to normal. During the episode, they are unaware of their surroundings and won’t respond. These typically only lasts 10-20 seconds. Most patients (> 90%) stop having absence seizures as they get older.
Management is: sodium valproate or ethosuximide
Summarise atonic seizures:
Atonic seizures are also known as “drop attacks”. They are characterised by brief lapses in muscle tone. These don’t usually last more than 3 minutes. They typically begin in childhood. They may be indicative of Lennox-Gastaut syndrome.
Management is:
- First line: sodium valproate
- Second line: lamotrigine
Summarise myoclonic
Myoclonic seizures present as sudden brief muscle contractions, like a sudden “jump”. The patient usually remains awake during the episode. They occur in various forms of epilepsy but typically happen in children as part of juvenile myoclonic epilepsy.
What is ‘West syndrome’?
West syndrome aka infantile spasms is a rare (1 in 4000) disorder starting in infancy at around 6 months of age. It is characterised by clusters of full-body spasms. There is a poor prognosis: 1/3 die by age 25, however, 1/3 are seizure-free. It can be difficult to treat but first-line treatments are:
- Prednisolone
- Vigabatrin
Complications of sodium valproate:
- Teratogenic so patients need careful advice about contraception
- Liver damage and hepatitis
- Hair loss
- Tremor
There are a lot of warnings about the teratogenic effects of sodium valproate and NICE updated its guidelines in 2018 to reflect this. It must be avoided in girls or women unless there are no suitable alternatives and strict criteria are met to ensure they do not get pregnant.
Describe the muscle weakness seen in Bell’s Palsy:
Acute (but not sudden) onset, unilateral, lower motor neuron facial weakness, sparing the extraocular muscles and muscles of mastication.
What features are suggestive of Ramsay hunt syndrome in place of Bell’s palsy?
Features particularly suggestive of Ramsay-Hunt Syndrome include: prominent otalgia, and vesicular rash in the external auditory meatus, palate or tongue.
Damage to what nerve presents with foot drop?
Common fibular nerve (common peroneal nerve)
The common peroneal nerve winds round the head of the fibula and is commonly damaged with fractures of the fibular head. It supplies the tibialis anterior muscle (via it’s branch the deep peroneal nerve). This muscle dorsiflexes the ankle and therefore damage to its innervation leads to foot drop.
UFC!
Explain how status epilepticus is defined but also approached!
Status epilepticus is defined as a seizure lasting >5 minutes, or multiple seizures over 5 minutes with incomplete resolution.
Guidelines have changed
How is early status epilepticus treated?
- If in the community:
- Buccal Midazolam or Rectal Diazepam
- If IV access is obtained and resuscitation facilities are available:
- Lorazepam (intravenous) 0.1 mg/kg (usually a 4 mg bolus, repeated once after 10−20 minutes; rate not critical).
How is established status epilepticus (0-60mins) treated if not responding to 2 doses of benzodiazepine, give any of the following as second-line treatment
- Levitiracetam
- Phenytoin
- Sodium Valproate
How is refractory status treated? (30-90mins)
- General anaesthesia, with one of:
- Propofol (1–2 mg/kg bolus, then 2–10 mg/kg/hour) titrated to effect
- Midazolam (0.1–0.2 mg/kg bolus, then 0.05–0.5 mg/kg/hour) titrated to effect
- Thiopental sodium (3–5 mg/kg bolus, then 3–5 mg/kg/hour) titrated to effect; after 2–3 days infusion rate needs reduction as fat stores are saturated
- Anaesthetic continued for 12−24 hours after the last clinical or electrographic seizure, then dose tapered.
What are the most important initial investigations to do in someone presenting with status?
Blood sugar and O2 sats
The most important initial investigations are to check the patient’s oxygen saturations and blood sugar level, as these are a common and rapidly reversible cause of seizure activity.
Additional management for status in an alcoholic?
IV pabrinex prior to the administration of glucose to avoid precipitation of Wernicke’s encephalopathy or Korsakoff’s syndrome.
Note additional investigations that should be carried out in status:
First line blood tests should include an arterial blood gas, and a routine panel of venous bloods including FBC, U&E, LFT, CRP, Calcium and magnesium, and clotting. Patients should have a serum and urine save for toxicology, and antiepileptic drug levels should be sent as appropriate.
Treatment for GBS?
Immunoglobulin and Plasmapheresis are the treatment options, ideally before the ascending weakness causes paralysis of respiration. The sensory disturbance described is dysaesthesia which is also seen in GBS.
What is GBS and what is it caused by?
GBS is an ascending inflammatory demyelinating polyneuropathy.
Typically 1-3 weeks after infection (e.g. Campylobacter, mycoplasma, EBV). 40% of cases are idiopathic.
How does GBS present?
Progressive ascending symmetrical limb weakness (affecting the lower limbs first). Paraesthesia may precede the onset of motor symptoms. Respiratory muscles may be affected in severe cases. Some cases present with symptoms of cranial nerve palsies (e.g. diplopia, facial droop).
Lower motor neurone signs in the lower limbs (hypotonia, flaccid paralysis, areflexia). Cranial nerve signs may also be present (e.g. ophthalmoplegia, lower motor neurone facial nerve palsy, bulbar palsy) as well as signs of type 2 respiratory failure due to respiratory muscle weakness (e.g. CO2 flap, bounding pulse). Autonomic dysfunction may be present (e.g. arrhythmia, labile blood pressure).
Investigations carried out for GBS:
Bedside tests include spirometry (checking for a reduced FVC). Bloods include an ABG (to check for type 2 respiratory failure) and anti-ganglioside antibodies. Other investigations include a lumbar puncture which typically shows a raised protein, with normal cell counts and glucose (so called albuminocytological dissociation).
What is Miller-Fisher syndrome?
Miller-Fisher syndrome is a variant of GBS that presents with ataxia, ophthalmoplegia, and areflexia.
The condition is typically positive for anti-GQ1b antibodies.
Malingering
Malingering is the deliberate faking of symptoms in order to obtain secondary gain.
What is the most common form of occupational focal dystonia?
Writer’s cramp is the most common form of occupational focal dystonia. It typically only occurs with a specific action. Dystonia is a sustained muscle contraction often with slow, twisting or repetitive movements or abnormal postures
Management for myasthenia gravis:
Management is with prednisolone (acutely) and cholinesterase inhibitors e.g. pyridostigmine or neostigmine (long-term)
Management for myasthenia gravis:
Management is with prednisolone (acutely) and cholinesterase inhibitors e.g. pyridostigmine or neostigmine (long-term)
How to distinguish an L5 root lesion from a common fibular (peroneal) nerve palsy:
The isolated loss of ankle eversion and dorsiflexion are most consistent with a common fibular nerve palsy. Loss of inversion and sensory disturbance in addition would suggest an L5 root lesion.
What is the tetrad seen in Wernicke’s encephalopathy?
Confusion, ataxia, nystagmus and opthalmoplegia.
What happens if Wernicke’s encephalopathy is left untreated.
Left untreated, the condition can progress to Korsakoff’s syndrome. This syndrome affects the mammillary bodies to cause irreversible deficits in anterograde and retrograde memory.
Issues with phenytoin:
Need to be very careful with the dose and requires cardiac monitoring.
Definition of SE:
Seizure lasting more than 5 minutes or multiple seizures lasting more than 5 mins without ROC.
Summarise the key features of temporal arteritis:
Temporal arteritis (also known as giant cell arteritis: GCA) is a vasculitis of unknown cause that affects medium and large-sized vessels arteries. It occurs in those over 50 years old, with a peak incidence in patients who are in their 70s.
It requires early recognition and treatment to minimize the risk of complications such as permanent loss of vision. Hence, when temporal arteritis is suspected, treatment must be started promptly with high-dose prednisolone as well as urgent referral for assessment by a specialist.
There is an overlap between temporal arteritis and polymyalgia rheumatica (PMR) - around 50% of patients will have features of PMR.
Features of temporal arteritis:
- typically patient > 60 years old
- usually rapid onset (e.g. < 1 month)
- headache (found in 85%)
- jaw claudication (65%)
- tender, palpable temporal artery
- around 50% have features of PMR: aching, morning stiffness in proximal limb muscles (not weakness)
- also lethargy, depression, low-grade fever, anorexia, night sweats.
What investigations are carried out for temporal arteritis?
- raised inflammatory markers
- ESR > 50 mm/hr (note ESR < 30 in 10% of patients)
- CRP may also be elevated
- temporal artery biopsy
- skip lesions may be present
- note creatine kinase and EMG normal
Summarise the three treatment principles for treating temporal arteritis:
- High dose prednisolone
- Referral to ophthalmology (urgent same day as visual damage is irreversible).
- Bone protection with bisphosphonates is required as long, tapering the course of steroids is required.
Summarise trigeminal neuralgia and it common causes:
Trigeminal neuralgia is a pain syndrome characterised by severe unilateral pain. The vast majority of cases are idiopathic but compression of the trigeminal roots by tumours or vascular problems may occur.
Red flag symptoms in trigeminal neuralgia:
- Sensory changes
- Deafness or other ear problems
- History of the skin or oral lesions that could spread perineurally
- Pain only in the ophthalmic division of the trigeminal nerve (eye socket, forehead, and nose), or bilaterally
- Optic neuritis
- A family history of multiple sclerosis
- Age of onset before 40 years
Diagnosis and investigations carried out for trigeminal neuralgia:
Clinical diagnosis. Can consider an MRI head to look for nerve compression if needed.
Trigeminal neuralgia managment:
- carbamazepine is first-line
- failure to respond to treatment or atypical features (e.g. < 50 years old) should prompt referral to neurology
Differentials of a subarachnoid haemorrhage:
▪ Subarachnoid haemorrhage
▪ Other intracranial hhge incl
pituitary apoplexy
▪ Dissection of cerebral blood
vessels
▪ Cerebral vasculitis
▪ Reversible cerebral
vasoconstriction syndromes
▪ Cerebral venous sinus thrombosis
▪ Idiopathic
▪ Raised temperature
▪ Neck stiffness
▪ Seizures
▪ Alteration in consciousness
Differentials:
CNS Infection:
▪ Meningitis- bacterial , viral
▪ Encephalitis- seizures , alteration in consciousness
▪ Cerebral Abscess
▪ Subdural empyema
▪ Paraspinal collections
▪ Unusual organisms
▪ Systemic infection can also cause associated headache
What are the investigations carried out in a suspected CNS infection?
▪ Start antibiotics/ antivirals
▪ CT Brain
▪ DO NOT delay an LP if no contraindications
▪ MR brain in encephalitis –temporal lobe changes /
hhge
Raised ICP features:
▪ Headaches worsening on lying down or waking a patient from sleep
▪ Brought on by Valsalva
▪ Visual obscurations- maybe accompanied by pulsatile tinnitus
▪ Papilloedema
▪ Diplopia from a 4th or 6th nerve palsy
Differentials of a headache with features of a raised ICP:
▪ Tumours
▪ Cerebral venous sinus thrombosis
▪ Malignant meningitis
▪ Significant Chiari malformation
Features of IIH:
Classical clinical features include headache and visual disturbance.
The headache is classically non-pulsatile, bilateral, and worse in the morning (after lying down or bending forwards).
Treatment summary for IIH:
First line management of idiopathic intracranial hypertension (and the only intervention supported by good evidence) is weight loss.
Failing this, patients often try carbonic anhydrase inhibitors, such as acetazolamide, but its extensive profile of side effects (peripheral paraesthesia, anorexia and metallic dysgeusia) mean that it is poorly tolerated.
Topiramate is also commonly used for headache prophylaxis.
More invasive strategies to lower CSF pressure including therapeutic lumbar punctures and surgical CSF shunting are tried in resistant cases.
In patients with prominent visual symptoms (but otherwise manageable headaches), optic nerve sheath fenestration may protect against visual loss.
Essential investigations for headaches with raised ICP features:
▪ CT brain+ contrast and
venogram
OR
▪ MRI brain and venogram
Temporal arteritis summary:
– Jaw claudication
– Stroke like features
– Raised infl markers
– Along with starting steroids a temporal
artery biopsy has to be arranged to happen
as early as possible ( preferably within 48
hours- 7 days )
Diagnostic criteria for episodic migraine:
▪ Diagnostic criteria:
▪ A. At least 5 attacks fulfilling criteria B–D
▪ B. Headache attacks lasting 4–72 hours (untreated or unsuccessfully treated)
▪ C. Headache has at least two of the following characteristics:
– 1. unilateral location
– 2. pulsating quality
– 3. moderate or severe pain intensity
– 4. aggravation by or causing avoidance of routine physical activity (eg, walking or climbing stairs)
▪ D. During headache at least one of the following:
– 1. nausea and/or vomiting
– 2. photophobia and phonophobia
▪ E. Not attributed to another disorder
What causes the aura in a migraine?
Under functioning of the cerebral cortex.
Forehead sparing stroke vs bell’s palsy
Stroke spares
Bell’s palsy includes paralysis of the forehead
What is meant by ophthalmoplegia?
Ophthalmoplegia, also called extraocular muscle palsy, paralysis of the extraocular muscles that control the movements of the eye. Ophthalmoplegia usually involves the third (oculomotor), fourth (trochlear), or sixth (abducens) cranial nerves. Double vision is the characteristic symptom in all three cases.
Anterograde vs retrograde memory loss:
Anterograde: This kind of memory loss means you can’t form new memories. This word partly comes from the Latin word “ante,” which means before. In this context, a person can’t store memories moving forward. Retrograde: This kind of memory loss means you lose memories from your past.
What serious complication to be aware of with patients on lamotrigine?
Development of a rash - SJS!!
What are category 1 anti-epileptics?
Give two examples:
Anti-epileptics that require you to stay on the same brand.
- Phenytoin and carbamazepine.
Risk of a patient with epilepsy taking tramadol?
Lowers seizure threshold.
Ciprofloxacin does this too.
What is the only medication licensed to treat MND?
Riluzole is the only medication licensed for the treatment of motor neuron disease, and extends life expectancy by around three months
Explain the use of thrombolysis for stroke.
Thrombolysis is the definitive treatment in a patient with ischaemic stroke confirmed by CT head scan who has presented sooner than 4.5 hours after symptom onset.
What antibodies are most commonly seen in MG patients?
Antibodies to post-synaptic acetylcholine receptors (Anti-AChR)
Explain the surgical management of mystasthenia gravis.
Surgical management with thymectomy is considered in some patients. Myasthenia gravis is associated with thymic hyperplasia (65% of patients) and thymoma (12% of patients). Evidence suggests thymectomy leads to symptom improvement in 50% of patients and remission in 25% of patients.
What scoring system is used to quantify the risk of stroke?
CHA2DS2VASc
Explain the CHA2DS2VASc score system:
C - Congestive Heart Failure
H - Hypertension
A - >75 years (Scores 2)
D - Diabetes
S - Previous stroke/TIA (Scores 2)
V - Vascular disease
A - 65-74 years
Sc - Sex (Female scores 1).
A score of 0 indicates low risk and anticoagulation may not be considered. A score of 1 indicates low-moderate risk and anticoagulation should be considered. A score of greater than 2 indicated high risk and anticoagulation should be started when weighed against bleeding risk.
What is the clinical triad seen in optic neuritis:
- Visual loss
- Periocular
- Dyschromatopsia
What is the reversal agent for dabigatran?
Idarucizumab
What is the genetic cause of Friedreich’s ataxia
This is caused by a triple repeat in the FXN gene encoding the frataxin protein.
Trinucleotide repeat disorder.
Signs of a cerebellar stroke
DANISH
Surgical clipping treats what brain bleed?
Subarachnoid haemorrhage
Surgical treatment for EDH:
Craniotomy + evacuation
Ligation of the bleeding artery may stem the blood flow and prevent the haemorrhage from worsening or reoccurring
Treatment for patients with acute ischaemic stroke with large vessel occlusion?
Thrombectomy
Endovascular coiling is a surgical intervention to treat what?
Subarachnoid haemorrhage
Summary of a posterior circulation stroke:
This can present with vertigo, ataxia and dysarthria due to involvement of the vestibular and cerebellar systems.
If he is within the 4.5h window, alteplase should be rapidly administered, in the absence of contraindications. CT head must be performed beforehand to rule out a haemorrhage
Most common thromboembolic stroke?
MCA - middle cerebral artery
Initial investigation for SAH
NON-CONTRAST CT
CT findings for hemorrhagic stroke:
Haemorrhagic stroke: HYPER-dense area on CT
CT findings for ischaemic stroke:
Ischaemic stroke: HYPO-dense area on CT
How to differentiate L5 radiculopathy with foot drop:
The main differentiating factor between L5 radiculopathy and common peroneal nerve palsy is still being able to invert the foot in common peroneal nerve palsy. It presents as a foot drop, foot eversion weakness and sensory loss to the lateral aspect of the thigh.
What information is carried in the dorsal column?
The sensory modalities of fine touch (tactile sensation), vibration and proprioception.
Where does the dorsal column deccusate?
Medulla oblongata
What information is carried in the anterior spinothalamic tract?
Anterior spinothalamic tract– carries the sensory modalities of crude touch and pressure.
What information is carried in the lateral spinothalamic tract?
Lateral spinothalamic tract – carries the sensory modalities of pain and temperature.
Where does decussation occur in the spinothalamic tract occur?
Spinal cord (first order neurones enter the spinal cord, ascend 1-2 vertebral levels, and synapse at the tip of the dorsal horn and decussate across the spinal cord).
Features of SAH:
Thunderclap
Syncope
Vomitting
Neurological weakness
Ophthalmoplegia
Neck stiffness
Indications of headache due to raised ICP:
Worse when lying / waking from sleep
Brought on by valsalva
Pulsatile tinnitus
Papilloedema
Diplopia (due to 4th or 6th nerve palsy)
What is normal csf pressure?
<25cm
When to consider IIH?
– Diagnosis of exclusion
– Only to be considered in the appropriate population of patients
– Papilloedema
– Ophthalmology assessment with fields
– Normal CT or MR brain and venogram
– LP - CSF opening pressure measured in the relaxed decubitus position is > 25 cm
– CSF analysis normal
Investigations for headache with raised ICP features:
▪ CT brain+ contrast and
venogram
OR
▪ MRI brain and venogram
Describe MS in 5 words!
Multifocal UMN disorder
Symptoms of cerebral venous sinus thrombosis:
Headache, seizure, papilloedema, reduced GCS, focal deficit.
Headache 82%
Reduced GCS 31%
Papilloedema 50%
Cranial nerve palsies 11% (II- VII)
Seizure(s) 42%
Bilateral cortical signs 4%
Focal deficit 41%
Cerebellar signs 3%
Investigations for cerebral venous sinus thrombosis:
CTV or MRI Venogram
What is meant by an orthostatic headache?
Headache onset within 5- 15 minutes of sitting up or standing up severe ( very often throbbing ) bilateral severe headache which is incapacitating.
Can occur spontaneously or due to LP.
Note the positional element is lost in chronic cases.
Managment of a secondary headache due to low CSF pressure:
▪ Lie flat (complete recovery is 1-2 weeks).
▪ IV fluids 8 hourly or 2-3 litres of oral fluids/ 24 hours
▪ Takes a good 1-2 weeks to recover fully
▪ In the spontaneous type- MR brain with contrast
▪ If patients are worsening despite medical treatment for 72 hours –epidural blood patch
Jaw claudication is highly suggestive of…
Temporal arteritis
Summary of Temporal arteritis:
Features, inv, and managment.
– Jaw claudication
– Stroke like features
– Raised infl markers
– Along with starting steroids a temporal artery biopsy has to be arranged to happen as early as possible ( preferably within 48 hours- 7 days )
Headaches red flags
– New neurological deficit
– Immunocompromised
– Known malignancy
– Elderly
– Anticoagulated
– Pregnancy
- B symptoms
Diagnostic criteria for migraine:
▪ A. At least 5 attacks fulfilling criteria B–D
▪ B. Headache attacks lasting 4–72 hours (untreated or unsuccessfully treated)
▪ C. Headache has at least two of the following characteristics:
– 1. unilateral location
– 2. pulsating quality
– 3. moderate or severe pain intensity
– 4. aggravation by or causing avoidance of routine physical activity (eg, walking or climbing stairs)
▪ D. During headache at least one of the following:
– 1. nausea and/or vomiting
– 2. photophobia and phonophobia8
▪ E. Not attributed to another disorder
What medications are given to manage migraine acutely?
Triptan (e.g sumitriptan)
NSAID (ibuprofen)
Antiemetic (if needed)
How to importantly screen for medication overuse headache in a history:
More than 10-15 doses of medication being used a month.
How to identify if a patient is suffering with chronic migraine?
Duration >3months
8 days a month has features of migraine
Triggers: stress, fatigue, sleep disturbance, dehydration, hormones, missing meals.
Suitable prophylaxis for chronic migraine:
▪ Propranalol (20-240 mg )
▪ Amitryptiline/ Nortryptiline (10- 100 mg)
▪ Topiramate (50-200 mg)
▪ Pregabalin ( 75-600 mg )
▪ Candesartan ( 4- 16 mg )
What are the three main trigeminal autonomic cephalgia’s?
Cluster headache
Hemicrania
SUNCT / SUNA
What is SUNCT?
Short lasting Unilateral Neuralgiform headache with Conjunctival Tearing
Lasts a few seconds 100’s of times a day
Note: Has autonomic symptoms.
Frequency of attacks of hemicrania:
30 minute attacks 20 times a day
Features of cluster headaches:
Considered a medical emergency!
▪ Unilateral, Side locked headaches. Severe pain,
▪ Autonomic symptoms (streaming of the eye and nostril, conjunctival congestion, swelling of face eyelids )
▪ Night time attacks waking pt up from sleep usually 2-6 am
▪ Severe agitation and restlessness
▪ Periodicity
Cluster headache treatment:
– Sumatriptan –injection / nasal spray.
– Oxygen 15L non-rebreather
Cluster headache long term prevention options:
– Verapamil –likely to need high doses between 480 mg - 960 mg/day -ECG monitoring
– Topiramate
– Lithium
What divisions of the trigeminal nerve are affected in trigeminal neuralgia?
2 and 3
Maxillary and mandibular
Causes of trigeminal neuralgia:
Compression of vascular loop
Tumours
MS
(Can investigate with MRI)
Management of trigeminal neuralgia:
Carbamazepine (usually very responsive)
Surgery - decompression / ablation
Refer to neuro
How is a diagnosis of MS made?
2 attacks with objective clinical evidence.
Note: With dissemination in space and time.
Causes of MS:
Genetics
Vitamin D insufficiency
EBV virus (small effect)
Weight/salt/smoking
Summarise the epidemiology of MS:
1/750 people affected in the UK.
Risk factors: Genetics, Vitamin D deficiency, EBV virus, lifestyle.
60% of patients have relapsing and remitting MS which go onto develop secondary progressive MS.
20% don’t progress (benign MS).
15% have primary progressive MS.
Prognosis of MS:
5yrs reduced life expectancy. Disease of morbidity not mortality.
30yrs from onset to wheelchair on average, 13yrs in progressive MS.
Explain what the symptoms of MS are?
- why are they so varied?
Balance/vertigo, fatigue, bladder dysfunction, spasticity, sensory dysfunction, pain, memory problems, eye/sight problems.
- MS causes damage anywhere in the CNS and so symptoms can be very diverse.
Treatment of acute relapse in MS
High dose methylprednisolone 500mg
Summarise the approach to managing MS treatment.
- Treat acute relapse - high dose methylprednisolone.
- Prevent relapse - interferon / dimethyl fumarate.
- Prevent progression - ongoing studies.
- Neural repair? - science fiction atm.
Treat the symptoms.
What causes long term disability in MS?
Progression! Episodes of relapse do not necessarily lead to long term disability.
Encephalitis causative organism:
HSV 1
A patient has failure to adduct on the right side, and nystagmus in the left side.
- what’s the diagnosis?
Right internuclear ophthalmoplegia
- failure to adduct the affected side and nystagmus in the contralateral side.
Causes of internuclear ophthalmoplegia:
- Vascular (e.g. Stroke)
- Demyelination (e.g. Multiple Sclerosis): This is more commonly bilateral
Medication to prevent cluster headaches:
Verapamil
First line treatment for trigmeminal neuralgia:
Carbamazepine
Treatment for carotid stenosis?
Carotid endarterectomy
1st line treatment for absence seizures in an 8yr boy?
Sodium valproate
MRI finding in encephalitis:
BILATERAL medial temporal lobe involvement.
1st line treatment for focal seizures:
Leviteracetam or lamotrigine.
How does bulbar MND present?
Early tongue involvement and bulbar symptoms.
What are bulbar symptoms?
Lip trembling.
Drooling – inability to swallow, saliva gathers in mouth.
Dysphonia – vocal cord paralysis results in rasping voice.
Difficulty in articulating.
Weak jaw, facial muscles.
Pharyngeal muscle weakness.
Key presenting feature of progressive muscular atrophy?
Only lower motor neuron features.
Key presenting feature of primary lateral sclerosis?
Only upper motor neuron features.
Clinical features of spinal ALS:
Classically, there is a combination of upper motor neuron and lower motor neuron signs.
Upper motor neuron signs include spasticity, hyperreflexia and upgoing plantars (though they are often down going in MND).
Lower motor neuron signs include fasciculations, and later atrophy.
Generally, the eye and sphincter muscles are spared until late in the disease course and sensory disturbance is NOT seen (and should prompt consideration of an alternative diagnosis).
What key features does Brown-sequard syndrome present with?
- Ipsilateral hemiplegia
- Ipsilateral loss of proprioception and vibration
- Contralateral loss of pain and temperature sensation
Caused by hemisection of the spinal cord.
DANISH
Cerebellar dysfunction:
Dysdiadochokinesia (inability to perform rapid alternating movements)
Ataxia
Nystagmus (typically multidirectional)
Intention tremor (tremor during voluntary movement illustrated by the finger-nose test)
Slurred speech
Hypotonia
Medication to manage chorea in Huntington’s patients?
Tetrabenazine
Side effects of topiramate:
Weight loss
Renal stones
Cognitive and behaviour changes
Teratogenic
Parkinsonism and vertical gaze palsy =
Progressive supranuclear palsy
Most common visual field defect in MS:
This patient’s background of multiple sclerosis and presentation of peri-orbital pain and vision loss is highly suggestive of optic neuritis. Although optic neuritis can present with various visual field defects, a central scotoma is the most common.
Timeline for thrombolysing a stroke patient:
Thrombolysis is the definitive treatment in a patient with ischaemic stroke who has presented sooner than 4.5 hours after symptom onset.
Imaging for myasthenia gravis:
CT Chest
Myasthenia gravis is strongly associated with abnormalities of the thymus, and imaging to look for thymic hyperplasia or thymoma is warranted to evaluate the role of thymectomy
Presentation of Wernicke’s:
Wernicke’s often presents with an alcohol history along with a triad of confusion, ataxia, and ophthalmoplegia. Sometimes, there can be postural hypotension or hypothermia too
Why can you invert the foot in a common peroneal nerve palsy?
Inversion is controlled by tibialis posterior and anterior which is innervated by the tibial nerve.
What histopathological feature is seen in Parkinson’s disease?
Lewy body depositions with alpha synuclein protein.
What histopathological feature is seen in Parkinson’s disease?
Lewy body depositions with alpha synuclein protein.
Motor features of Parkinson’s:
Bradykinesia, asymmetric resting tremor, rigidity, postural instability.
Shuffling gait, reduced facial expression, reduced arm swing.
Non-motor features of Parkinson’s:
Constipation, depression, psychosis, ED, REM behavioural disorders, cognitive decline, anosmia.
Positive muscle-specific tyrosine kinase antibodies are seen in what condition?
Myasthenia Gravis
A saccular aneurysm is associated with what type of brain bleed?
SAH
What are the features of multiple system atrophy?
Parkinsonism and early autonomic clinical features such as: postural hypotension, incontinence, and impotence.
When are anticholinergics used in IPD?
Used in tremor-dominant PD.
Side effects of anticholinergic medications:
Dry eyes and mouth
Constipation
Urinary retention
How do COMT inhibitors work?
- name two commonly used.
The COMT inhibitors, tolcapone and entacapone, are a new class of Parkinson’s medications.
By inhibiting the enzyme catechol-o-methyl-transferase (COMT), they prevent peripheral degradation of levodopa, allowing a higher concentration to cross the blood-brain barrier.
Where does deep brain stimulation stimulate in the brain to treat parkinson’s?
Globus pallidus and subthalamic nucleus
Explain vascular/atypical parkinsonism:
Sometimes referred to as lower half parkinsonism.
- Predominant gait and postural instability.
- Poor levodopa responsiveness.
- Control cerebrovascular risk factors (smoking, high BP, DM, dyslipidaemia).
CT/MRI may show multiple infarcts.
Summarise Lewy body dementia:
LBD is parkinson’s symptoms + cognitive symptoms within one year of motor symptoms.
-visual hallucination + fluctuating cognition.
- alpha synuclein
Summarise progressive supranuclear palsy:
Has features of early falls, postural instability, vertical gaze palsy.
- Rocket’s sign - falling backwards on standing from a chair.
Summarise multiple system atrophy:
Parkinson’s features but characterised with autonomic dysfunction (impotence is an early sign in males).
- Features of ataxia plus parkinsonism.
- Feautres of orthostatic hypotension which is managed with high salt diet, midodrine and fludrocortisone.
Summarise corticobasal syndrome:
Limb apraxia, dystonia (cramps), myoclonus.
- Marked asymmetry at onset.
- Cognitive deficits: Visuospatial, acalculia (can’t process numbers), alien limb phenomenon.
- Cortical atrophy.
Differentials of Parkinsons:
PSP (LBD, vascular parkinsonism, drug induced, progressive supranuclear palsy, MSA).
Encephalitis
Frontal meningioma.
Diagnosis of parkinson’s:
Clinical: Bradykinesia + one of:
Asymmetric resting tremor
Rigidity
Postural instability
Imaging for Parkinson’s?
Only in unclear cases:
MRI to rule out other pathology e.g frontal meningioma, BG lesions, cerebellar changes).
DAT-spect (dopamine transporter scan.
Genetic testing - can aid genetic counselling.
Absent ankle reflex with foot drop = likely what
L5 radiculopathy
Postural instability, impairment of vertical gaze, parkinsonism, frontal lobe dysfunction = ???
Progressive supranuclear palsy
Vertical diplopia when reading in bed = what cranial nerve is affected?
Trochlear
The trochlear nerve innervates the superior oblique muscle which abducts, depresses and internally rotates the eye. Therefore the affected eye is unable to look down as easily, therefore causing vertical diplopia, worst on looking down (whilst reading).
1st line for generalised epilepsy
Sodium valproate
1st line medication for a focal seizure
Lamotrigine
1st line medication for a pregnant patient with epilepsy
Lamotrigine
What ophthalmic complication is seen in GCA?
Anterior ischaemic optic neuropathy is caused by inflammation in the posterior ciliary artery (a branch of the ophthalmic artery) which leads to occlusion and subsequent ischaemia to the head of the optic nerve.
What sign differentiates between organic and functional lower leg weakness?
Hoover’s sign
What is Hoover’s sign?
Hoover’s sign of leg paresis is a specific manoeuvre used to distinguish between an organic and non-organic paresis of a particular leg. This is based on the concept of synergistic contraction. If a patient is genuinely making an effort, the examiner would feel the ‘normal’ limb pushing downwards against their hand as the patient tries to lift the ‘weak’ leg. Noticing this is indicative of an underlying organic cause of the paresis. If the examiner, however, fails to feel the ‘normal’ limb pushing downwards as the patient tries to raise their ‘weak’ leg, then this is suggestive of an underlying functional weakness, also known as ‘conversion disorder’.
Parkinson’s tetrad + incontinence + orthostatic hypotension =
Multiple system atrophy
Wernicke’s Aphasia is due to a lesion where?
Superior temporal gyrus
Broaca’s Aphasia is due to a lesion where?
Left inferior frontal gyrus
Common complication of SAH (endo).
SIADH is a common consequence of subarachnoid haemorrhage.
- SIADH leads to hyponatremia and therefore symptoms of low sodium including nausea, vomiting, headaches, muscle cramps, and reduced consciousness.
Donepezil - is what class of drug?
acetylcholinesterase inhibitor
Parkinson’s medication that causes a pathological gambling/impulse control disorders
Dopamine agonists eg. bromocriptine, ropinirole, cabergoline, apomorphine
GCA effect on the eye and fundoscopy finding
Anterior ischemic optic neuropathy - fundoscopy typically shows a swollen pale disc and blurred margins.
First line tx in diabetic neuropathy?
Amitriptyline
Duloxetine
Gabapentin
Pregabalin
(Any of the above. Treatment is monotherapy so swap medications if one doesn’t work).
How to differentiate acute vs chronic subdural brain bleeds on CT?
Chronic subdurals arehypodense (dark)compared to the substance of the brain as the blood has aged and lost density.
Acute subdurals will present as a bright hyperdense crescenteric bleed.
How do acute on chronic subdural bleeds appear on CT?
There is active extravasation into the clotted blood, which gives you a ‘swirl’ sign of dark blood surrounded by bright blood, this is an ‘acute on chronic’ bleed.
What is the earliest sign of MS?
Lethargy is a very common early symptom of multiple sclerosis.
SAH CT modality?
CT head WITHOUT contrast
What is diagnostic first line for MS?
MRI brain
A 72-year-old man is brought to clinic by his family. They are very concerned about his declining cognition. He was normally very well and independent until 3 months ago. He has lost no weight, has no headache but has been falling a lot. He also complains of urinary incontinence.
Hold on…
Is that the triad of urinary incontinence, gait instability and dementia?
= Normal pressure hydrocephalus
Management of normal pressure hydrocephalus:
Ventriculoperitoneal shunting
Around 10% of patients who have shunts experience significant complications such as seizures, infection and intracerebral haemorrhages
Bamford Stroke Classification:
- Unilateral weakness, (plus/minus century deficit) .
- Homonymous hemianopia
- Higher cerebral dysfunction (e.g dysphasia).
Anterior circulation stroke
Note:
Total = all 3 symptoms
Partial = 2 symptoms
Features of an anterior circulation stroke:
- Unilateral weakness, (plus/minus century deficit) .
- Homonymous hemianopia
- Higher cerebral dysfunction (e.g dysphasia).
Bamford Stroke Classification:
1. CN palsy + unilateral motor/sensory deficit.
2. Bilateral motor/sensory deficit.
3. Eye movement disorders.
4. Cerebellar symptoms.
5. Isolated homonymous hemianopia
Posterior circulation stroke
Symptoms of a posterior circulation stroke (Bamford classification).
- CN palsy + unilateral motor/sensory deficit.
- Bilateral motor/sensory deficit.
- Eye movement disorders.
- Cerebellar symptoms.
- Isolated homonymous hemianopia (macular sparing)
Bamford stroke classification:
- Sensory only, motor only or sensorimotor.
Lacunar syndrome
Presentation of an ANTERIOR CEREBRAL ARTERY STROKE
Anterior cerebral artery stroke causes leg weakness but not face weakness or speech impairment
Middle cerebral artery stroke features
An infarct here would present with the upper limb being affected more than the lower limb and may have associated aphasia, which is not seen in an ACA infarct.
Features of a posterior cerebral artery stroke:
This presents with homonymous hemianopia with macular sparing and visual agnosia. CN affected.
Posterior inferior cerebellar artery stroke features:
If this artery is affected, it leads to a lateral medullary syndrome which is characterised by ipsilateral facial pain loss and temperature loss and contralateral limb/torso pain loss with temperature loss as the spinothalamic tract is affected.
Aka Wallenbergs!
Anterior inferior cerebellar artery (lateral pontine syndrome) stroke features:
Ipsilateral: facial paralysis and deafness
How does a lacunar stroke present?
present with either isolated hemiparesis, hemisensory loss or hemiparesis with limb ataxia
strong association with hypertension
common sites include the basal ganglia, thalamus and internal capsule
Management of autonomic dysreflexia:
Management of autonomic dysreflexia involves removal/control of the stimulus and treatment of any life-threatening hypertension and/or bradycardia.
Cape-like loss of pain and temperature sensation due to compression of the spinothalamic tract fibres decussating in the anterior white commissure of the spine describes what condition?
Syringomyelia
Side effects of SODIUM VALPROATE
Sodium = Hyponatraemia
V - VALPROATE:
A - Appetite increase –> weight gain
L - Liver failure
P - Pancreatitis
R - Reversible hair loss (alopecia)
O - Oedema
A - Ataxia
T - Teratogenic, tremor, thrombocytopaenia
E - Enzyme inducer (p450), encephalopathy (due to high ammonia)
Treatment for a medication overuse headache (assume patient has been overusing paracetamol, sumatriptan, codeine).
Medication overuse headache
• simple analgesia + triptans: stop abruptly
• opioid analgesia: withdraw gradually
Neuro complications of sinusitis:
seizure after acute sinusitis PLUS;
- Focal Neurology - Cerebral Abscess
- Cranial Nerve Palsy, Ophthalmoplegia - Cavernous Sinus Thrombosis
- Neck Stiffness, Photophobia, Kernig’s/Brudzinski’s positive - Meningitis
Other complications
- Painful Ophthalmoplegia, Proptosis, Eye swelling - Orbital Cellulitis
- Staph. Aureus - Associated with increased risk of frontal bone osteomyelitis
Seizure type with floaters and flashes
Occipital
Seizure type with paraesthesia
Parietal
Midbrain stroke characterised by the an ipsilateral CN III palsy and contralateral hemiparesis
Weber’s syndrome
What is seen on bloods in neuroleptic malignant syndrome?
Raised CK leukocytosis
How do lacunae strokes present?
unilateral motor disturbance affecting the face, arm or leg or all 3.
complete one sided sensory loss.
ataxia hemiparesis.
vertigo, hearing loss, tinnitus and an absent corneal reflex =
Vestibular Schwanoma
MS imaging
MRI WITH CONTRAST
Additional management after giving steroids for Bell’s palsy?
Artificial tears and taping shut the eye
Paralysis, low GCS, and bilateral pinpoint pupils are characteristic of what?
Pontine haemorrhage
Ropinirole mechanism of action:
Dopamine agonist
Superior homonymous quadrantanopias are caused by lesions where?
Superior homonymous quadrantanopias are caused by lesions of the inferior optic radiations in the temporal lobe.
How do anterior cerebral artery strokes present?
(ACA) strokes are characterised by:
Contralateral hemiparesis and sensory loss with the lower extremity being more affected than the upper.
How do anterior inferior cerebellar strokes present?
AICA strokes often present with sudden-onset vertigo and vomiting, ipsilateral facial paralysis, and deafness.
How do middle cerebral artery strokes present?
(MCA) strokes are the most common, but they would typically present with contralateral hemiparesis and sensory loss with the upper extremity being more affected than the lower, contralateral homonymous hemianopia, and aphasia.
What causes lateral medullary syndrome?
Lateral medullary syndrome is caused by posterior inferior cerebellar artery strokes (PICA).
Anterior cerebral artery stroke causes what symptoms?
Anterior cerebral artery stroke causes leg weakness but not face weakness or speech impairment.
Sudden onset vertigo and vomiting, ipsilateral facial paralysis and deafness - anterior inferior cerebellar artery
IPSILATERAL facial paralysis!! AICA with cerebellar signs and deafness.
Patients with GBS may have pain where?
Back/leg pain is seen in the majority of patients with Guillain-Barre syndrome
Back/leg pain is seen in the majority of patients with Guillain-Barre syndrome
Back and leg pain = make GBS a differential to rule out!!
Broaca’s lobe is located where?
Frontal lobe
Wernicke’s is located where?
Temporal lobe
For MS you need an MRI brain WITH CONTRAST.
- you always forget this so what type of contrast do they use for MS?
CONTRAST USED IN MS because it shows inflammation better!
Suspected optic neuritis: MRI of the brain and orbits with gadolinium contrast is the investigation of choice.
What differentiates Korsakoff’s from Wernickes?
An inability to acquire new memories and confabulation suggests the development of Korsakoff’s syndrome.
Always replace vitamin B12 before folate - giving folate to a patient deficient in B12 can precipitate subacute combined degeneration of the cord
Started on folate recently more sus of Subacute CDC!
Define GBS:
GBS is an ascending inflammatory demyelinating polyneuropathy that presents with lower motor neurone signs affecting the lower limbs.
Hemicrania continua tx
Indomethacin
Which anti-epileptic is most associated with weight gain?
Sodium valproate may cause weight gain
Carbamazepine to treat what…
Trigeminal neuralgia
Treatment of NEAD
- Trauma therapy / General CBT
- Treatment for mood disturbance / anxiety.
Define tetraparesis
Weakness in all four limbs aka quadraparesis
Paresis = weak
Plegia = paralysis
Inv for GBS
Spirometry FVC!
ABG - T2 resp failure?
LP shows raised protein, normal cell count, glucose normal
NERVE CONDUCTION STUDIES and EMG!
What do nerve conduction studies assess?
- used to confirm GBS diagnosis
- Speed of impulse (slower in GBS due to demyelination)
- Amplitude (lower in GBS)
GBS treatment
IVIg and plasmapharesis
Tetrabenazine is used for what?
To manage chorea in Huntington’s patients.
Dimethyl fumarate is used for what?
Prevent relapse in MS
Syringomyelia presentations
Syringomyelia classically presents with cape-like loss of pain and temperature sensation due to compression of the spinothalamic tract fibres decussating in the anterior white commissure of the spine.
Investigation syringomyelia
MRI
What is EMG?
Electromyography - tests muscle response to an electrical impulse
2nd line stroke prevention is clopidogrel not tolerated:
clopidogrel is contraindicated or not tolerated, give aspirin and modified release dipyramidole for secondary prevention following stroke
What is meant by the munro kelli doctrine?
Blood flow to the brain is directly proportional to the resistance in the arteries and inversely proportional to the blood pressure.
CPP = (Neuro theme)
CPP (Cerebral perfusion pressure) = MAP - ICP.
The standard HbA1c target in type 2 diabetes mellitus is what?
48 mmol/mol
Recent travel abroad: Splenomegaly, Spots, Slow HR
Typhoid fever
