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.
