Neurology Lectures Flashcards
Describe the physiology of consciousness
Anatomically consciousness is dependent on the reticular activating system in the brain stem and the cerebral cortex. Biochemically this is dependent on GABA-type A receptors, NMDA and noradrenaline receptors.
Define Coma
Coma is defined as the total absence of awareness of both self and the external environment. It is a state of hypnosis, amnesia, areflexia, and analgesia. The patient will not open their eyes to the pain, do not move spontaneously, and do not utter recognizable words.
Describe the causes of loss of consciousness
Loss of consciousness can be caused by a vast array of conditions. These can be remembered by:
Units of Insulin
Narcotics
Convulsions
Oxygen
Non-organic
Stroke
Cocktail
ICP
Organism (infection)
Urea
Shock
CO2 and CO excess
Overdose
Metabolic
Apoplexy
How should an unconscious patient by assessed?
When assessing an unconscious patient, always start with the airway. Reduced level of consciousness is the number one cause of airway obstruction. This may require airway manoeuvres, airway adjuncts or intubation. This may present as snoring.
Breathing should be assessed as always for increased or reduced effort of breathing. Always considered whether oxygen or ventilation support is required. This may also indicate the cause of LOC such as overdose or CO poisoning.
Circulation assessment should be assessed for inadequacies or arrhythmias.
GCS or AVPU score should be used for disability. Pupils should be assessed here:
- Small reactive pupils: Metabolic encephalopathy or midbrain herniation
- PP/Fixed: Pontine lesion, opiates or organophosphates
- Dilated/reactive: Metabolic, midbrain, ecstasy or amphet’s
- Dilated/Fixed: Ictal, hypoxia, ischaemia, hypothermia, or anticholinergics
- Unequal: Horner’s, III nerve palsy or Uncal herniation
Everything else should assess rash, pyrexia, evidence of trauma, PMH and even what is in their pockets.
What investigations should be done for the unconscious patient?
Investigations should include blood gases, bloods, BMs, urine dip, or other special tests.
Describe some specialist treatments for the unconscious patient when the cause is hypoglycemia or opiate overdose
Hypoglycemia should be treated with 10% glucose if unconscious. Pabanex should be given alongside this if there is evidence of alcohol abuse to avoid Wernicke’s Korsakoff’s. Opiate overdose should be treated with naloxone 200 or 200mcg IV.
How does SAH present?
Subarachnoid hemorrhage shows a star sign of CT. 50% will have a warning bleed which presents as a sudden onset severe headache, this will go away. 1/3 develop during exercise. Risk factors include a FMx, smoking, hypertension, and connective tissue disease. They may have a III or VI nerve palsy, papilledema, or signs of meningism. Subarachnoid Haemorrhage is assessed with the Hunt and Hess score or the World Federation of Neurosurgeons score.
How should SAH be managed?
Subarachnoid heamorrhage patients should be transferred to a specialist neurological centre, given analgesia + antiemetics, surgical clipping, ICP monitoring, BP management and Nimodipine po 60mg/ 4hrly (within 48 hours of the bleed).
Rebleeding occurs in 4% within 48 hours and 20% within 2 weeks. This is associated with a high mortality. SH is also associated with subdural haemorrhage, global cerebral ischaemia, vasospasm (hence nimodipine), hydrocephalus, seizures and SIADH/cerebral salt wasting syndrome.
Describe the epidemiology of brain tumours
Primary brain tumours are uncommon at 12,000 a year but they are increasing in the UK. Brain tumours are second most common tumour in children behind haematological malignancy.
What are the causes of brain tumours?
Causes of brain tumours can include hereditary syndromes such as neurofibromatosis or tuberous sclerosis, immunosuppression (HIV/AIDS) leading to cerebral lymphoma, and therapeutic ionizing radiation. There is no correlation with a head injury, power lines, smoking, or air pollution.
What are the most common brain tumours and how are they graded?
The three most common brain tumours are meningioma (benign), glioblastoma (primary malignancy) and metastases which are often solitary with surrounding oedema. WHO classification of brain tumours is based on the appearance of the cell such as glia – glioma. Gliomas can include astrocytoma, oligodendroglioma and ependymoma.
Grading is based on the WHO classification:
1. Pilocytic astrocytoma (most common in children)
2. Diffuse astrocytoma
3. Anaplastic astrocytoma
4. Glioblastoma (most aggressive primary)
Oligodendromas can only be classified as type 2 or 3 (anaplastic). These have a fried egg appearance. Patients respond well to treatment.
Meningiomas have three grades:
1. Meningioma
2. Atypical
3. Anaplastic (malignant)
Resection is usually curative.
Once the tumour has been named and graded, genetics should be considered:
- 1p 19q deletion = Oligodendroglioma (better prognosis)
- IDH1 mutation = Astrocytoma (better prognosis with mutation)
- MGMT promotor methylation = Glioblastoma which respond to chemotherapy
- P53 mutation = Gliomas
Describe the behaviour of benign brain tumours
Benign brain tumours behave differently in the brain. Some invade surrounding brain/blood vessels/tissues. Therefore, patients still die of benign tumours so they should be called pre-malignant.
Describe primary malignant brain tumours and metastases to the brain
Primary malignant tumours of the brain tend to spread throughout the brain and rarely to other parts of the body. Metastases to the brain are from lung (small cell most common), breast, melanoma, renal and colorectal. 1/3 will be solitary metastases, 1/3 up to 4 and 1/3 numerous. Metastases usually spread to the cerebrum (80%), cerebellum (15%) and the brain stem (5%).
How do brain tumours present?
Presenting symptoms include headache, nausea and vomiting, blurred vision (papilledema), fits, dysphagia, progressive weakness or numbness, sudden deterioration from a bleed or it may be an incidental finding. Always check for signs of a metastases from elsewhere in the history.
How should patients with a suspected brain tumour be assessed initially?
Assess the performance score to understand what the aim of treatment is for each individual patient. Patients who are able to care for themselves are most likely to benefit from treatment. 1% of patients are diagnosed on 2 week wait. Most patients present through ED.
Consider an urgent direct access MRI in adults with progressive subacute loss of CNS function – NICE
In children – consider a very urgent referral (48 hours) with newly abnormal cerebellar or other central neurological function.
What investigations should be ordered for a suspected brain tumour?
Bloods: FBC, U&Es, LFTs, Clotting, CEA, PSA, aFP, prolactin and IGF1. These should all be normal.
Imaging:
- CT will show an abnormal lesion
- MR is the best imaging as it shows anatomy better and spectroscopy can be done to assess cell turnover. Blood flow can also be assessed as angiogenesis is an indicator of neoplasia. Surgical planning can also be done with MR as speech tracts can be viewed.
- Functional MR looks at primary cortical areas which light up when movement are instigated. This is assess by blood oxygen level dependent as blood moves to the area of the brain which is in use. This allows for the damage of resection to be determined.
- Positron Emission Tomography (PET) can help assess new tumour growth vs response to treatment.
Histology is the ultimate determining investigation.
How should brain tumours be treated?
Biopsy should be done if operation is not possible. This is then discussed at MDT. Surgery may not always be curative but will assist with prognosis and quality of life in most cases. It can also help improve the outcome of chemotherapy or radiotherapy.
Gliomas produce migrating cells which may proliferate in years to come. Further, some cells may respond to chemotherapy whereas others don’t in the same tumour.
Metastases to the brain should be treated depending on the assessment of performance. The type of metastases is rarely important.
Awake surgery is useful when tumours are near speech areas as this allows surgeons to improve outcomes. 5 ALA is a drink given before operation which lights up tumour tissue under UV light so more can be resected.
Gliadel is chemotherapy in wafers that can be inserted during surgery near the tumour resection site.
The mainstay of tumour treatment is radiotherapy and radiosurgery. Radiotherapy is with fractionated treatment over 6 weeks every day. This is prognostically beneficial for all patients (temozolamide). Radiosurgery is a single dose treatment is excellent for metastases and meningiomas.
What are the prognostic factors for brain tumours?
Prognostic factors include age, radiotherapy, surgery, and chemotherapy. Many patients take cannabis oil, laser therapy, ketogenic diet and tumour treating fields (electric fields) are all unknown options.
What is the DVLA guidance for those with brain tumours?
DVLA guidance is that brain tumour patients are not allowed to drive. This is a 2 year ban for grade III or IV (malignant), 1 year for low grade and 6 months for symptomatic meningioma. No ban for asymptomatic meningioma.
Define meningitis and how does it present?
Meningitis is inflammation of the meninges and presents with headache, vomiting, photophobia, neck stiffness and Kernig’s sign
What is encephalitis and how does it present?
Encephalitis is a viral invasion/inflammation of brain tissue. This presents with behavioural change, psychiatric illness, confusion, coma, focal signs and convulsions
What is an brain abscess and how does it present?
An abscess is a space-occupying lesion and thus presents with focal neurology
Define myelitis and how does it present?
Myelitis is inflammation of the anterior horn cells in the spinal cord. This can present with flaccid limb paralysis and absent reflexes.
What is encephalopathy?
Encephalopathy is a clinical syndrome of altered mental status manifesting as reduced consciousness or altered cognition, personality, or behaviour. This has many causes including systemic infection, toxins, hypoxia, trauma, vasculitis, or CNS infection.
How is encephalitis diagnosed and how can the cause be determined?
Encephalitis is inflammation of the brain. This is strictly a pathological diagnosis, but clinical markers are used such as CSF inflammatory change or changes in neuroimaging. Causes include viruses, small intracellular bacteria and some parasites. Rarely it can be caused by disseminated encephalitis myelitis (ADEM) or antibody-associated encephalitis.
When assessing cognitive status you can use assessment tools such as MOCA (Montreal cognitive assessment) or ACE (Addenbrooke’s cognitive assessment).
Movement disorders in encephalitis suggest an autoimmune cause, especially orofacial movements or chorea. If a rash is present consider shingles or if purpura it may be meningococcus. Animal or insect bites may suggest rabies or malaria.
How should a patient with a suspected brain infection be investigated?
Any patient with a suspected brain infection should have an LP and CSF analysis. This is essential for distinguishing brain infection from systemic infection. If there is evidence of ‘brain shift’ then a CT should be done before LP. Signs of ‘brain shift’ include focal neurology other than cranial nerves, papilledema, recent onset seizures, moderate-severe impairment of consciousness, hypertension with bradycardia, or immunocompromise. Other contraindications for an LP include bleeding disorders, anticoagulant treatment and sepsis over the spine.
‘Brain shift’ is a concern because it pushes the brain down and an LP will cause herniation and coning. On CT a brain shift will present with loss of normal sulcal patterns and reduced space around the basal cisterns.
The CSF should then be sent for PCR
How is epilepsy defined?
A transient occurrence of signs and/or symptoms due to abnormal, excessive or synchronous neuronal activity in the brain.
Seizures can be classified as focal onset, generalised onset, or unknown onset.
This is a disorder of the brain characterised by an enduring predisposition to generate epileptic seizures and by the neurobiological, cognitive, psychological, and social consequences of this condition.
How is epilepsy diagnosed?
Diagnosis of epilepsy:
- At least two unprovoked seizures occurring greater than 24 hours apart
- One unprovoked seizure and a probability of further seizures similar to the general recurrence risk (greater than 60%) after two unprovoked seizures, occurring over the next 10 years – e.g one seizure with structural abnormality or abnormal EEG.
- Diagnosis of epilepsy can be given concurrently to the diagnosis of an epilepsy syndrome
Epilepsy classification is based on seizure type (focal, generalised or unknown), epilepsy type (focal, generalised, combined or unknown), Epilepsy syndrome (clusters of features such as generic generalised epilepsies) and aetiology (structural, generic, infectious, metabolic, immune or unknown).
What are the causes of epilepsy?
Birth trauma, genetic (cerebral dysgenesis, tuberous sclerosis, and storage diseases), congenital infections, cerebral tumours, intracranial infections, febrile seizures, head injuries, hypoglycaemia, hypocalcaemia, pyridoxine dependency, drugs and alcohol and cerebrovascular degeneration.
It is important to establish whether there are primary brain tumours, metastases, AV malformations, and infarction.
Describe the onset of epilepsy and its prognosis
Generalized onset epilepsies are usually present in childhood whereas focal/partial epilepsies present later in life (usually acquired causes). The prognosis for epilepsy is that 70% will become seizure-free with antiepileptics whereas 40% will be without treatment. Epilepsy which is not controlled by anti-epileptics is refractory.
How should convulsions be assessed in a clinical setting?
- Differentiate between seizures and seizure mimics (syncope, sleep disorders, migraine, paroxysmal movement disorders, and psychological disorders)
- Differentiate between acute symptomatic seizures and unprovoked (spontaneous) seizures
- Classify seizure type and epilepsy type. Basic history and examination, ECG, bloods, and glucose. If focal consider MRI and then EEG whereas generalised should have EEG.
Convulsions can be caused by seizures, concussive convulsions, syncope, and dissociative seizures.
How should syncope and seizures be differentiated?
Syncope: Upright posture, pallor and sweating, gradual onset, no injury, can have convulsive jerks, rarely incontinent, unconsciousness lasting for a few seconds, recovery is rapid, no post-ictal confusion, occur infrequently and are often preceded by lack of food or unpleasant circumstances
Seizures: Any posture, no pallor or sweating, sudden onset (sometimes with aura), can have an injury, convulsive jerks, commonly incontinent, unconsciousness lasting minutes, recovery is slow, post-ictal confusion, frequent seizures and rarely any precipitating factors
Acute symptomatic seizures are almost always tonic-clonic. They can be:
- Metabolic disturbance such as uraemic/hepatic encephalopathy, electrolyte disturbance, DKA, severe illness, drugs, or alcohol (withdrawal or intoxication)
- CNS disorders such as trauma, surgery, haemorrhage, infection, and cerebral hypoxia
What advice should be given to new-onset epilepsy patients?
All patients should be offered a diagnosis and explanation, discuss triggers (poor sleep and alcohol), safety, status epilepticus, and SUDEP risk, driving advice, and consider discussions around pregnancy and breastfeeding.
What is status epilepticus?
Status epilepticus is a seizure that lasts longer than 5 minutes or having more than 1 seizure within a 5 minute period without returning to normal level of consciousness.
What is SUDEP?
SUDEP stands for Sudden, Unexpected Death in Epilepsy
What are the medical options for epilepsy treatment?
1.Focal epilepsy – generally give Lamotrigine
2.Generalised epilepsy – Sodium Valproate (never in pregnancy) or lamotrigine in women of childbearing age
Epilepsy should be treated with monotherapy. Rational polytherapy means prescribing drugs with different mechanisms of action if one is not sufficient.
Refractory epilepsy is defined as the failure of adequate trials of two appropriate and adequately tolerated AEDs, either as monotherapy or polytherapy. These patients may be considered for epilepsy surgery.
What are the surgical options for epilepsy management?
Epilepsy surgery is indicated in patients with focal epilepsy that is medically refractive, non-eloquent cortex, no significant medical/psychiatric co-morbidities and fully counselled.
Surgical options include focal resection (temporal lobe resection or extratemporal resections of the frontal, parietal or occipital lobe), lesionectomy, multiple subpial transections, laser interstitial thermal therapy, anatomical or functional hemispherectomy/hemispherotomy, corpus callosotomy or stereotactic radiosurgery.
What are the non-pharmacological options for managing epilepsy?
Nonpharmacological management includes vagal nerve stimulation (modest degree of benefit) or ketogenic diet (high fat, low carb diet to induce ketosis) is most effective in patients with epilepsy syndromes and refractory seizures.
How should epilepsy be managed in women of childbearing age
Women of childbearing age (15-45) – All must be on folic acid supplementation
AEDs have teratogenic risks and neurocognitive risks, but this should be measured against the dangers of uncontrolled seizures. Focal seizures are unlikely to have major impact on mother/fetus however generalised seizures can cause hypoxia, lactic acidosis, blunt trauma, reduction of IQ of child, and an increased risk of SUDEP.
AEDs, especially sodium valproate, has an increased risk (10%) of major congenital malformations. This risk is increased with polytherapy. There is also a significant reduction in IQ for children exposed to valproate in utero where lamotrigine and levetiracetam have less/no impact.
How do AEDs affect breastfeeding?
In breastfeeding there is no adverse effects for taking AEDs when breastfeeding. Lamotrigine metabolism is affected by pregnancy and the dose may need to be increased during pregnancy.
Describe a primary and secondary headache
Primary headache has no underlying physical abnormality
Secondary headaches are due to an underlying abnormality or an external factor. These account for less than 1% of presentations to GP. They present with a sudden onset severe headache (thunderclap). Other red flags are signs of CNS infection, raised or low cranial pressure, new onset neurological deficit, alteration of consciousness, elderly, known malignancy, immunocompromised, head injury, anticoagulated, glaucoma, or temporal arteritis
Describe a typical history for a thunderclap headache
Thunderclap headache is defined as a new sudden onset headache which is severe right from the onset. There will not be any build up to the symptoms. Associated symptoms such as syncope or vomiting are relevant. There may be ophthalmoplegia or true neurological weakness. The location of the pain is not always relevant unless behind the eye or back of the neck.
What are the causes of a thunderclap headache?
Causes include subarachnoid haemorrhage (usually berry aneurysm), other intracranial haemorrhages such as pituitary apoplexy, dissection of cerebral blood vessels, cerebral vasculitis, reversible cerebral vasoconstriction syndrome, cerebral venous thrombosis, and idiopathic causes.
How should a thunderclap headache be investigated and treated?
A CT brain scan must be done immediately. If CT does not show a reason for thunderclap headache, then 12 hours later an LP and CSF examination should be done. The 12-hour gap is so that blood not picked up on CT can break down into bilirubin and then be detected on the xanthochromia test.
Subarachnoid hemorrhage should be treated with IV or enteral nimodipine, a short course of tranexamic acid, VTE assessment, fluid therapy, and potentially surgical review of the ruptured aneurysm.
How does a CNS infection with thunderclap headache present?
Cardinal features are raised temperature, neck stiffness, seizures, and alteration in consciousness. Causes include meningitis, encephalitis, cerebral abscess, subdural empyema, paraspinal collections, unusual organisms, and systemic infection with associated headache.
How should a thunderclap headache caused by CNS infection be managed?
Management is to start antibiotics/antivirals, CT brain, DO NOT delay an LP if there are no contraindications and MR brain if suspecting encephalitis for temporal lobe changes or haemorrhage.
What would a thunderclap headache with raised CSF present with?
There will be headaches AND papilledema/loss of visual acuity/visual field defect/ new IV or VI nerve palsy. Headache which are worse on lying down or waking up, and those brought on by Valsalva manoeuvres (not worsened) should be considered worrying. A feeling of pressure or tightness is not relevant. Visual obscurations are loss/clouding of vision with valsalva and they may also have pulsatile tinnitus.
What are the causes of raised CSF headaches?
Causes of raised CSF headaches include tumours, cerebral venous sinus thrombosis, malignant meningitis (cancer cells), and significant Chiari malformations. IIH is a diagnosis and should only be considered in appropriate young overweight individuals. They may have papilledema, normal CT, MRU and venogram, CSF analysis normal but CSF opening pressure high.
How should raised CSF headaches be investigated?
When suspecting raised ICP, CT brain with contrast and venogram or MRI brain and venogram. This will pick up most of the secondary causes of papilledema.
Describe the features of a cerebral venous sinus thrombosis
Cerebral venous sinus thrombosis presents with headache, papilledema, seizures, focal deficit, reduced GCS, cranial nerve palsies, bilateral cortical signs, and rarely cerebellar signs. Precipitating causes include trauma, intracranial tumour, infection, abscess, meningitis, post-partum, oral contraceptive pill, polycythaemia, systemic infection and severe dehydration. The headache can be progressive over days or be thunderclap. These patients require a CT with venogram or MRI with venogram.
How does a low CSF headache present?
Low CSF pressure occurs post lumbar or dural puncture. Rarely they are spontaneous. They will not have a headache on lying down but within 5-15 minutes of sitting up or standing they will have severe (throbbing), bilateral severe headache which is incapaciting. Orthostatic headaches. The positional element is lost in chronic cases.
How should low CSF pressure headaches be treated?
Treatment is to lie flat (symptomatic relief) for days-week and let the tear heal. This will heal in around a week but will worsen if they try to go about their daily activities. Patient should have IV fluids 8 hourly or 2-3 litres of oral fluids every 24 hours. If spontaneous in origin then a MR brain with contrast is needed to look for a cause and if patients are worsening despite medical treatment for 72 hours then epidural blood patch is required.
Describe some other headache red flags
1.New headache with neurological deficit/immunocompromised/known malignancy/elderly/anticoagulated/pregnancy
2.Temporal arteritis which presents with jaw claudication, stroke like features, and raised inflammatory markers. These patients should be started on steroids and a temporal artery biopsy should be arrived within 2-7 days. Jaw claudication is pain on chewing caused by temporal ischaemia to the temporalis and masseter. Usually in patients over 50.
3.Glaucoma presents with loss of vision and halo effect. They require emergency ophthalmology assessment.
All of these patients with new sudden onset headache have a high risk of persistent headaches which behaviour like chronic migraine.
Describe migraine
Migraine is a form of sensory processing disturbance with manifestations within and outside the CNS function. The trigemino-cervical complex is currently the accepted pathway of migraine genesis. Pain is only one of the symptoms. The TCC pathophysiology involves a variety of neuropeptides in a cascade. There is a genetic predisposition with genetic types with aura such as FMH and CADASIL. Frequent migraines is a tendency rather than a disease.
What are episodic migraines?
Episodic migraine is episodes of headaches that can be unilateral or bilateral (1-4 days) which are moderate-severe intensity and involve the face, scalp and neck. The pain may be aching/throbbing/stabbing/pressure-like. Patients may have nausea, photophobia, noise sensitivity and olfactory sensitivity. It affects the patient’s capacity to function as they will prefer to lie down, sleep, and keep away from noise. In between episodes they will function well and be free of symptoms.
Diagnostic criteria is at least 5 headaches fulfilling:
1. Duration 4-72 hours
2. Headache has two of the following: Unilateral, pulsatile, moderate/severe pain and avoidance of routine activity
3. One of the following during the headache: Nausea or vomiting or photophobia or phonophobia
Aura occurs in 20%. This is a spreading neurological deficit that can affect visual, sensory, and speech but will completely reverse after coming on over 5 minutes. Black spots in front of the eyes is not aura.
What are the phases of migraine?
Phases:
- Premonitory (days): yawning, craving, mood changes and hypothalamic
- Aura phase (2-60 mins) with cortical spreading dysfunction
- Headache phase (up to 3 days) with the TCC firing
- Postdrome (days) with a dull persistent headache, TCC firing and central sensitisation.
How should acute migraine be treated?
Acute episodes should be treated with triptans AND/OR aspirin OR NSAIDs as first line. Ensure adequate hydration, aim to reduce pain by 50%, do not use opiates and advise patient to recuperate at home with rest and use pain medications sparingly. Migraine sufferers should be evaluated for use of preventative therapy if they are getting more than 2-3 episodes a month or if the episodes are severe.
Very severe attacks should be treated with triptans, NSAIDs and antiemetics. Avoid opiates and codeine.
What is chronic migraine?
Chronic migraine occurs after many years of episodic migraine with progression. It is defined as headache occurring on 15 or more days/month for more than three months or 8 days a month with features of migraine. Triggers include stress, fatigue, sleep disturbance, dehydration, hormones and missing meals.
If patients use analgesia for more than 10 days in a month that will make the migraines worse.
How should chronic migraine be managed?
Management of chronic migraine:
-Explain that this is a long process which may take 6-9 months
-Try to get patients off regular analgesia and start them on preventatives
-Use short courses of naproxen to help patients come off codeine
-Rest, hydration and avoiding triggers
-Refer to neurology if not benefitting from adequate trials of three or more preventatives
Preventative options include propranolol, topiramate, pregabalin and candesartan. Doses should start small and work up. Make take 3-4 months to work. Other options are calcium antagonists, SSRIs, occipital nerve injections and acupuncture. Rarely botulinum toxin can be used.
What are trigeminal autonomic cephalgias?
Trigeminal autonomic cephalagias are always unilateral. The have prominent autonomic features because there is parasympathetic involvement due to being parallel to the trigeminal nerve. These symptoms include congestion or watering of the eye, eyelid drooping/swelling, blocked or runny nose. The patient will be restless and agitated. The headaches are episodic. The attacks are stereotyped as in they occur in exactly the same way every time (especially cluster). They are categorised by duration of attacks and frequency. Cluster is 1-8 attacks in 24 hours with each attack 1-4 hours, hemicrania are 30-minute attacks up to 20 times a day whereas SUNCT lasts for a few seconds for 100s times a day.
What are cluster headaches?
Cluster headaches are unilateral, side locked, headaches with extreme pain. They present with autonomic features such as streaming of the eye and nostril, conjunctival congestion, and swelling of the eyelids or face. Usually have night-time attacks which wake the patient up between 2-6am. There will be severe agitation and restlessness. There is periodicity as in they occur for a few weeks then go away.
How should cluster headaches be treated?
This is an emergency. Acute treatment is with sumatriptan (injection or nasal spray) and high flow oxygen (15 litres) through tight non-re-breathable mask via a HOOD form. Short term prevention is with greater occipital nerve blocks, prednisolone 60-80mg/day for 5 days and then taper off. This should not be done more than twice a year. Long term prevention is with verapamil (high doses of 480mg and ECG monitoring), topiramate, lithium and gammacore device. These patients should be referred to neurology.
What is trigeminal neuralgia?
This is a primary headache which affects the 2nd and 3rd trigeminal branches whereas cluster and migraine affect the 1st division. All headache pains are mediated by the trigeminal nerve. There will be recurrent paroxysms (jabs) of pain with triggers, a refractory phase and then remissions. Persistent dull ache of the face is not trigeminal neuralgia.
What are the causes of trigeminal neuralgia?
Trigeminal neuralgia can be caused by compression of the vascular loop/ tumours/ MS plaques. MRI will find a secondary cause in 5%. Vascular compression at the root of entry zone of the nerve can be demonstrated in 50% of idiopathic TNs.
How should trigeminal neuralgia be treated?
TN responds very well to Carbamazepine, but facial pain will not. Other options include phenytoin, gabapentin, pregabalin, lamotrigine, baclofen, and levetiracetam.
Define multiple sclerosis
Multiple sclerosis is defined as a multifocal UMN disorder, disseminating in time and space which can either be relapsing or progressive.
What is the pathophysiology of MS?
The pathophysiology of the inflammation is that there is focal demyelination which causes perivascular inflammation. On CT they are described as dawson’s fingers with white lesions spreading out from the ventricles. The position of the inflammatory lesion determines the symptoms which are experienced. For example:
-Weakness of both legs = spinal cord
-Numbness down the whole left arm = (right) cerebrum
-Dizziness, slurred speech, falls and left sided incoordination = brainstem (left cerebrum)
-Blurred vision in the left eye with painful eye movements = Cerebrum (left optic nerve). This is the only pain felt in MS.
How is MS diagnosed?
A diagnosis is made from 2 attacks with objective clinical evidence. This cannot be the same symptom as that would not be disseminated in space (of the brain).
What are the other risk factors for developing MS?
There is an increased risk with a family history of MS. There is also an association with low vitamin D, especially below the age of 14. EBV also has a small increased risk. Weight, salt and smoking may have a role
