Neurology Flashcards
Define Bell’s palsy?
Bell’s palsy is an idiopathic syndrome that causes damage to the facial nerve leading to a lower motor neuron facial palsy.
What causes Bell’s palsy?
The aetiology of Bell’s palsy remains unknown. Viral infections, particularly reactivation of herpes simplex virus type 1 (HSV-1), have been implicated as a possible cause.
Other viral pathogens, such as Epstein-Barr virus (EBV) and varicella-zoster virus (VZV), have also been suggested as potential triggers.
However, the exact mechanisms by which these viruses lead to facial nerve dysfunction are not fully understood.
Clinical features of Bell’s palsy?
Acute (but not sudden) onset of unilateral lower motor neuron facial weakness (classically affecting the forehead as this area has bilateral nervous supply from both sides of the brain)
Mild to moderate postauricular otalgia, which may precede the paralysis.
Hyperacusis
Nervus intermedius symptoms, such as altered taste and dry eyes/mouth.
Patients may subjectively describe “numbness” or “heaviness” without objective facial somatosensory disturbances.
What are the investigations for Bell’s palsy?
The diagnosis of Bell’s palsy is primarily clinical, based on the characteristic signs and symptoms.
However, in some cases, additional investigations may be considered to exclude other potential causes or to assess the severity of nerve dysfunction. These investigations may include:
Otoscopy to assess if any vesicular lesions are present in the external auditory meatus
Full blood count (FBC)
Erythrocyte sedimentation rate (ESR) or C-reactive protein (CRP)
Viral serology (e.g. HSV-1, EBV, VZV)
Lyme serology (if suggestive symptoms or exposure)
Electromyography (EMG)
Imaging studies (e.g. CT or MRI Head)
What is the short term management for Bell’s palsy?
The management of Bell’s palsy includes:
Prompt administration of oral steroids: 50mg of oral prednisolone or prednisone once daily for 10 days, followed by a taper.
Supportive treatments:
Artificial tears and ocular lubricants to manage dry eyes.
Eye patch/tape to prevent corneal exposure and injury.
What may be considered in treatment for Bell’s palsy?
Although the pathophysiology of Bell’s palsy has not been definitively linked to active herpes virus infection, empirical treatment with aciclovir may be considered, particularly in cases where the clinical distinction between Bell’s palsy and Ramsay-Hunt syndrome is difficult.
What is the long term management of Bell’s palsy?
Pain management with analgesics or anticonvulsants may be necessary in cases of severe otalgia or neuropathic pain.
Physical therapy, including facial exercises and massage, may be recommended to maintain muscle tone and prevent contractures during the recovery phase.
Psychological support and counseling may be beneficial for patients experiencing emotional distress or body image concerns due to facial weakness.
What percentage of patients with Bell’s palsy have a complete recovery?
Complete recovery: Approximately 70-80% of patients with Bell’s palsy achieve complete recovery of facial function without residual deficits.
Most improvement occurs within the first 3 months, with the greatest recovery seen within the first 6 weeks. However, some patients may continue to show gradual improvement even beyond this timeframe.
What two factors can decrease the likelihood of recovery for Bell’s palsy?
Age and severity: Older age and more severe initial facial weakness are associated with a higher risk of incomplete recovery.
Define a brain abscess?
A brain abscess is a collection of pus within the brain parenchyma. It is a very serious condition which can lead to significant morbidity and mortality, especially if left untreated.
What causes brain abscesses?
Brain abscesses are usually result from direct extension of an infection. This may be sinusitis, dental or cranial procedures or injury. Sometimes, the bacteria may spread through the bloodstream, for example a septic embolus from endocarditis. The most commonly isolated bacteria is Streptococcus, though other pathogens such as oral bacteria, Staphylococci, gram-negatives, TB, fungi and parasites can also cause brain abscesses, particularly in susceptible people
What are the signs and symptoms of brain abscesses?
Signs of infection: fever, nausea & vomiting, meningism
Raised intracranial pressure: headache, third nerve palsy, papilloedema, seizures
Focal neurology depending on location of abscess
What are the investigations for brain abscesses?
Bloods - including FBC, CRP, clotting, VBG, cultures
Cross-sectional imaging:
MRI is most sensitive for brain abscess, and will show an enhancing lesion.
If stroke is suspected, an urgent CT head will be required as per local pathways.
Neurosurgical aspiration/excision & cultures
What is the management for brain abscesses?
It is important to remember that when a patient is acutely unwell, start with an A-E assessment and consider initiating the sepsis six if the patient is showing signs. Call for help early - the exact team will depend on local protocols & clinical context. If the the patient is displaying acute neurological symptoms, initiate the stroke pathway as per local guidelines.
Exact management will be guided by seniors in neurology/neurosurgery & microbiology, but may include:
Neurosurgical intervention: aspiration or excision
Medical: antibiotics - initially a 3rd-generation cephalosporin + metronidazole. This may differ based on culture results and immune status of the patient. Typically, antibiotics continue for several weeks.
Symptom management - for example anticonvulsants for seizures, dexamethasone for severely raised intracranial pressure
What are the complications of brain abscesses?
Sepsis
Raised intracranial pressure & herniation
Permanent neurological deficits
Death
What are risk factors for brain abscesses?
Risk factors for brain abscess include:
Sinusitis
Dental, head & neck procedures
Cardiac defects & endocarditis
Poor immune response including HIV, immunocompromise
What would a CT reveal in a brain abscess?
ring enhancing lesion
Define brain metastases?
Brain metastases are secondary brain tumours that occur following spread from a tumour away from the central nervous system.
What causes brain metastases?
Malignancies usually spread to the brain haematogeneously. Cells seed into the brain’s small blood vessels and are often protected from anti-cancer therapies by the blood-brain barrier.
What are the most common primary malignancies that metastasise to the brain?
Lung cancer
Breast cancer
Colorectal cancer
Melanomas
Renal cell carcinoma
Signs and symptoms of brain metastases:
Brain metastases may occur in people with a known cancer, or may be their first presentation of malignancy. Symptoms can be due to local interruption of the nerve pathways or due to raised intracranial pressure. Key clinical features include:
Headaches
Seizures
Altered mental status, including confusion
Cerebellar signs, including ataxia
Nausea and vomiting
Visual disturbance
Focal neurology
Patients may also have signs of the primary malignancy, for example breathlessness and haemoptysis for lung cancer.
What are the investigations for brain metastases?
In a patient presenting with acute neurological features, it is important to rule out acute intracranial events, for example stroke. Therefore, a head CT is often employed first-line.
According to NICE, MRI is the best and initial imaging modality for diagnosing brain metastases. Further investigations may be necessary to identify the primary malignancy, for example chest imaging and biopsy.
What is the management for brain metastases?
Management of brain metastases requires a multidisciplinary approach. There are many factors to consider including the nature of the metastases, the patient’s age, performance status and primary tumour.
Systemic anti-cancer therapy is advised for people who have brain metastases likely to respond effectively, for example, germ cell tumours or small-cell lung cancer
Symptomatic management involves corticosteroids (usually dexamethasone) to reduce oedema, anti-seizure medications and antiemetics. Specific treatment for raised intracranial pressure may be necessary as well. Therapeutic options include radiotherapy (targeted, and sometimes whole-brain), chemotherapy and surgical resection.
Following treatment, patients will often have serial imaging follow up to assess any ongoing symptoms/potential progression
What is chronic fatigue syndrome also referred to as?
Myalgic encephalomyelitis
Define chronic fatigue syndrome?
CFS is a chronic illness characterised by persistent or recurrent fatigue that is not relieved by rest and is associated with significant functional impairment. It is a chronic multisystemic condition, with common features being post-exertional malaise, cognitive difficulties, unrefreshing sleep, autonomic dysfunction and pain. Symptoms should not be explained by any other cause.
The diagnosis should be suspected if fatigue has been present for at least 6 weeks with associated functional impairment, and symptoms are not secondary to another illness
Risk factors for chronic fatigue syndrome?
Risk factors include:
Family history
Epstein-Barr infection in adolescence
Covid-19 infection
How is chronic fatigue syndrome classified?
CFS can be classified by symptom severity
This is a way of approximating the impact of symptoms on daily life
However these categories are not clear-cut as symptoms may fluctuate in intensity and some symptoms may be more severe than others
There are additional management considerations for patients with severe or very severe CFS (see Management section for details)
What are the symptoms of mild chronic fatigue syndrome?
Patients are self-caring
May need some support with domestic tasks
Mobility may be affected
Often still in education or work, may need reduced hours and days off
Leisure and social activities usually curtailed
What are the symptoms of moderate chronic fatigue syndrome?
Restricted in all activities of daily living (ADLs)
Reduced mobility
Usually have stopped education or work
Sleep is usually poor quality
Rest periods usually needed
What are the symptoms of severe chronic fatigue syndrome?
No or minimal self-care (e.g. washing fash)
Mobility affected e.g. may require a wheelchair, often unable to leave the house
May spend most of the time in bed
Severe cognitive difficulties
Often hypersensitive to light and sound
What are the symptoms of very severe chronic fatigue?
Patients are bedbound
Dependent for all self-care including personal hygiene and eating
May require nutritional support (e.g. PEG feeding)
What are the signs and symptoms of chronic fatigue syndrome?
Patients should have all of the following symptoms, which have persistent over at least 3 months
Disabling fatigue
Worse on activity
Not significantly relieved by rest
Not due to excessive physical or mental exertion
Post-exertional malaise
Disproportionate to the activity
Prolonged e.g. may last days/weeks/longer
May be delayed in onset by hours/days
Sleeping difficulties
Sleep may be disturbed and/or unrefreshing
Patients may feel exhausted and stiff on waking
May have altered sleep pattern or hypersomnia
Cognitive difficulties
May describe “brain fog”
Poor concentration
Difficulties speaking or word-finding
Slow responses
Short-term memory impairment
What are the other symptoms of chronic fatigue syndrome?
Pain
May have generalised myalgia
May have headaches or eye/abdominal/joint pain
No signs of arthritis (e.g. erythema or swelling)
Being touched may be painful
Sensory sensitivities
e.g. to light/sound/taste/touch smell
May have temperature hypersensitivity (e.g. sweating/chills/hot flushes/feeling cold)
May be intolerant to alcohol/foods/certain chemicals
Autonomic dysfunction including orthostatic intolerance
Dizziness
Palpitations
Fainting
Nausea
Neuromuscular symptoms
Twitching or myoclonic jerks may be seen
Flu-like symptoms
Sore throat
Tender lymph nodes
Patients should be examined to look for signs of differential diagnoses
A mental state examination should be done to assess mood and cognition
Postural orthostatic tachycardia syndrome (POTS) may be seen (when the heart rate rises significantly when standing from lying down)
Postural hypotension may also be present
What investigations should we do for chronic fatigue syndrome?
There are no investigations that can diagnose CFS and the diagnosis is clinical.
However, all patients presenting with persistent fatigue should have the following blood tests to screen for an underlying physical cause:
Full blood count looking for anaemia, polycythaemia, inflammatory markers and haematological malignancy
U&Es for renal impairment or electrolyte imbalance
Liver function tests for liver disease
Bone profile to check calcium and phosphate
Myeloma screen especially in older patients or those with hypercalcaemia
Thyroid function tests for hypo or hyperthyroidism
HbA1c for diabetes
Ferritin which may be raised in inflammation or low in iron deficiency
ESR which is raised in inflammation or infection as well as some malignancies
Creatine kinase for muscle damage e.g. muscular dystrophy
IgA tissue transglutaminase for coeliac disease, which may present without gastrointestinal symptoms
What might urinalysis show in chronic fatigue syndrome?
Urinalysis should also be done, which may show glycosuria in diabetes, haematuria in renal tract inflammation, infection or malignancy, or proteinuria in inflammation or chronic kidney disease
Name some other random investigations based on clinical presentation for chronic fatigue syndrome?
Vitamin D in patients at risk of deficiency
Vitamin B12 and folate e.g. in anaemic patients or those with a restricted diet
Early morning cortisol to screen for adrenal insufficiency
HIV test in at risk patients (or all patients living in a high-prevalence area)
Hepatitis serology in at risk patients (e.g. those from an endemic area)
Monospot test for glandular fever in patients under the age of 40
Chest X-ray and sputum samples for tuberculosis in patients at risk (e.g. travel to an area where TB is endemic)
ELISA for Lyme disease if there is a history of tick bite
CT or MRI head if there are focal neurological signs or symptoms to rule out an intracranial cause for fatigue
Describe the management for chronic fatigue syndrome:
Management of CFS should be person-centred and tailored to individual needs
All patients should be referred to a specialist multidisciplinary team for confirmation of diagnosis and development of a care and support plan
Patients with severe/very severe CFS may require home visits for assessment and support
Advice should include:
Education on CFS and its management
Signposting to national and local resources and support
How to manage daily activity and not to “push through” symptoms of fatigue
Resting as much as needed (which may involve alterations to their daily activities)
Incorporating relaxation techniques into rest periods
Managing flare-ups and relapses
Maintaining a balanced diet and fluid intake
Developing good sleep habits
How to access social care support and assessment e.g. for disability benefits, adaptations to the home such as a stairlift
For moderate/severe/very severe CFS, consider the need for mobility aids (e.g. wheelchairs)
Support patients in work or education and ensure reasonable adjustments are put in place
Energy management is an important component of CFS care
This is a self-management strategy supported by the multidisciplinary team
Patients are encouraged to recognise their personal energy limits
Activities and rest periods should be planned accordingly
All types of activities including social, cognitive and physical should be considered
Plans should be regularly reviewed
Physiotherapy and occupational therapy input may be helpful for support with mobility and physical activity
Exercise programmes should be supported by specialist services for patients who would like to incorporate this into their CFS management
Cognitive behavioural therapy should be discussed
Patients are supported to manage symptoms, improve functioning and relieve distress
It is structured and time-limited
It focuses on the specific challenges faced by the patient
Comorbid conditions such as depression should be identified and managed
Associated symptoms such as orthostatic intolerance may require specialist input - this is usually managed with lifestyle changes; medications such as beta-blockers may be used
Additional investigations and analgesia may be required for pain management
Dietetic assessment is required for patients with weight loss or gain, those at risk of malnutrition e.g. due to a restrictive diet, or those with severe/very severe CFS
Vitamin D supplements should be considered for housebound patients
What are the complications for chronic fatigue syndrome?
Negative impacts on work, education, relationships and quality of life
Depression and/or anxiety
Malnutrition due to restrictive diet, poor appetite, food intolerances or difficulty with chewing/swallowing
Falls due to weakness and deconditioning
Pressure ulcers due to immobility
Deep vein thrombosis due to immobility
Contractures due to prolonged immobility
Vitamin D deficiency if leaving the house if difficult
Loss of earnings - 50% of patients with CFS have to stop work due to their symptoms
What is the prognosis for chronic fatigue syndrome?
Negative impacts on work, education, relationships and quality of life
Depression and/or anxiety
Malnutrition due to restrictive diet, poor appetite, food intolerances or difficulty with chewing/swallowing
Falls due to weakness and deconditioning
Pressure ulcers due to immobility
Deep vein thrombosis due to immobility
Contractures due to prolonged immobility
Vitamin D deficiency if leaving the house if difficult
Loss of earnings - 50% of patients with CFS have to stop work due to their symptoms
Define encephalitis:
Encephalitis is a pathological condition characterised by inflammation of the brain parenchyma.
What causes encephalitis?
The aetiology of encephalitis is predominantly viral, with the most common pathogen being the herpes simplex virus type 1 (HSV-1). Other viral causes can include HSV-2, enterovirus, cytomegalovirus, Epstein-Barr virus, varicella-zoster virus, HIV, and flaviviruses, including the West Nile virus.
Additionally, bacterial pathogens like those that cause meningitis, Lyme disease and Mycoplasma can cause meningoencephalitis. Parasitic infections with malaria or toxoplasmosis should be considered, especially with recent travel or immunocompromise. Autoimmune encephalitis, such as NMDA-receptor-antibody-associated encephalitis, should also be considered in the differential diagnosis.
Signs and symptoms of encephalitis?
Clinical features of encephalitis primarily include altered mental status, more so than in meningitis.
Other suggestive features include:
Fever
Flu-like prodromal illness
Seizures
Focal neurological deficits
Headaches
Behavioural changes
Meningismus
What is meningismus?
clinical syndrome of headache, neck stiffness, and photophobia, often with nausea and vomiting
What are the investigations for encephalitis?
Encephalitis should be suspected in any patient presenting with sudden onset behavioural changes, new seizures, and unexplained acute headache accompanied by meningism.
The standard work-up for encephalitis parallels that for meningitis and typically includes:
A routine panel of blood tests including FBC, U+E, LFTs (as part of a septic screen)
Blood cultures and viral PCR
Cerebrospinal fluid (CSF) analysis with viral PCR
Consideration for malaria blood films in cases of exposure
Central Nervous System (CNS) imaging through CT and MRI can provide valuable insight. For instance, HSV typically affects the temporal lobes and bilateral multifocal haemorrhage is typical.
Other tests may include sputum cultures, throat swab, chest X-ray and EEG (particularly if presenting with seizures)
What is the management for encephalitis?
Management of suspected encephalitis is empirical and involves broad-spectrum antimicrobial cover with 2g IV ceftriaxone BD and 10 mg/kg aciclovir TDS. Once the causative organism is identified, targeted treatment may begin.
Supportive management of complications is also crucial and can include the termination of seizure activity using anticonvulsants.
Acute encephalitis is a notifiable disease and should be reported to the local health protection team.
Ampicillin can also be added if Listeria monocytogenes is suspected
Define epilepsy?
Epilepsy is a neurological disorder characterised by an enduring predisposition to generate epileptic seizures and the neurobiological, cognitive, psychological, and social consequences of this condition.
Seizures are transient occurrences of signs and/or symptoms due to abnormal excessive or synchronous neuronal activity in the brain.
What causes epilepsy?
- Primary epilepsy is idiopathic
- Secondary causes:
- Tumour
- Meningitis
- Vasculitis
- Alcohol withdrawal
- Haemorrhage
- Metabolic
What conditions are associated with epilepsy?
- Cerebral palsy
- Tuberous sclerosis
- Mitochondrial disease
What type of seizures are there?
Focal seizure
Generalised Seizure
Status epilepticus
What is a focal seizure?
- Seizure localised to specific cortical regions
- May be complex (consciousness affected) or non-complex (consciousness not affected)
What is a generalised seizure?
Affects the whole brain and consciousness is lost immediately
- Absence
- Tonic
- Atonic
- Tonic-clonic
- Myoclonic
What is Status epilepticus and how do we treat?
seizure lasting longer than 5 minutes or ≥2 seizures within a 5-minute period without the person returning to normal between them
IV lorazepam or PR diazepam
Features of a frontal lobe focal seizure?
- Motor convulsions
- May show post-ictal flaccid weakness (post-ictal meaning just after seizure ends)
- Jacksonian march (clonic movements starting in 1 extremity and moving proximally through body) → usually starts as twitching/tingling of area like little toe or finger
Features of a temporal lobe focal seizure?
Most common type of partial seizure
- Aura- involving?
- Weird smells
- Involuntary movements
- Deja vu
- Abdo pain
- Lip smacking/plucking/grabbing (automatisms)
- Post-ictal dysphasia
- Hallucinations
Features of an occipital lobe seizure?
Visual disturbances (flashers and floaters)
Features of a parietal lobe seizure?
Sensory issues (paraesthesia- tingling, numbness)
Features of a tonic-clonic seizure?
- Vague symptoms before attack e.g. irritability
- Tonic phase (generalised muscle spasm- goes stiff and falls to floor)
- Clonic phase (repetitive synchronous jerks- jerking limbs or loss of bladder control)
- Urinary incontinence
- Tongue biting
- Post-ictal phase- including? (3)
- Impaired consciousness
- Lethargy
- Confusion
Features and treatment for an absence seizure?
- Onset in childhood
- Loss of consciousness but maintained posture (don’t fall down)
- No post-ictal phase
- Often begins abruptly without warning and ends abruptly
- Patient has no recollection of episode
- Stares blankly into space
3 Hz spike and wave
Treat with Ethosuximide
Features of myoclonic seizure?
- convulsions without the muscle tensing (tonic phase)
- Sudden jerking of limb, trunk or face with preserved consciousness
Features of atonic seizures?
- Sudden muscle relaxation causing patients to fall to the ground and then may motionless
- Can also result in incontinence
- Can result in post-ictal confusion
Features of a tonic seizure?
muscle tensing without convulsions (clonic phase)
General features of focal seizures?
With impaired consciousness (‘complex’): patients lose consciousness, usually post an aura or at seizure onset. Commonly originate from the temporal lobe, and post-ictal symptoms such as confusion are common.
Without impaired consciousness (‘simple’): patients retain consciousness, experiencing only focal symptoms. Post-ictal symptoms are absent.
Evolving to a bilateral, convulsive seizure (‘secondary generalised’): patients first experience a focal seizure that evolves into a generalized seizure, typically tonic-clonic
What is a Jacksonian march seizure?
A type of focal motor seizure that progressively ‘marches’ through adjacent areas of the brain
Typically starts in the hand or face then gradually spreads to other muscle groups following the smatotopic organisation of the motor cortex (starting from hand and spreading to arm, shoulder and face)
The seizure may progress into a generalised tonic clonic seizure
Often associated with structural brain lesions
What is Todd’s paresis?
Refers to temporary postictal weakness or paralysis following a seizure
Usually lasts minutes to hours but can last up to 48 hours
Usually unilateral but can be bilateral
It is transient so the patient will reover following resolution of the postictal state
What are the investigations for epilepsy?
Detailed history and neurological examination
Collateral history and, if present, reviewing any videos of previous episodes (with the patient’s consent)
Imaging such as CT or MRI
Electroencephalogram (EEG)
Video-EEG telemetry can also be considered in select cases
Other investigations can be considered to investigate contributory causes which include blood tests, lumbar puncture and more advanced imaging investigations.
What are the principles of epilepsy AGM management?
Aim for optimum quality of life through seizure control, balanced against potential side effects, particularly teratogenesis in women of childbearing age.
Initiation of medication may not always be appropriate after a “provoked” first seizure; discuss such cases with a specialist.
The choice of antiepileptic drugs involves complexity due to the lack of head-to-head trials comparing different medications.
Interactions with other medications, particularly with phenytoin and carbamazepine, should be considered.
Issues regarding teratogenicity, particularly with valproate, which carries a high risk of neural tube defects, should be considered. Lamotrigine is a better choice for women of childbearing age.
What two drugs should be considered as first-line for focal seizures?
Lamotrigine or Levetiracetam
What can be offered as first line for myoclonic seizures in males?
Sodium valproate
What is the drug choice for absence seizures?
ethosuximide
What drug may worsen myoclonic seizures
carbamazepine
What is the guidance for patients after the “first fit”
Usual protocols will advise to refer to outpatient neurology following a patient’s first seizure
Most neurologists would start an ASM after a second seizure, unless there is a specific structural cause or a second fit would be unacceptable to the patient.
Following a discussion regarding the risks and benefits of starting an ASM, patients are given information on reducing risks e.g. driving advice or taking showers rather than baths.
Patient education via leaflets or online websites are utilised heavily as part of the initial discussions and further follow up or advice is usually relayed via a dedicated epilepsy nurse
Name some complications of epilepsy?
Status epilepticus: Seizures lasting more than 5 minutes, necessitating immediate medical intervention OR more than 2 seizures within 5 minutes without returning to normal between each seizure.
Psychiatric complications: Increased risk of depression and suicide.
Sudden unexpected death in epilepsy (SUDEP): Thought to occur due to excessive electrical activity inducing a cardiac arrhythmia and subsequent death.
What are the side effects of topiramate?
Abdominal pain, cognitive impairment, confusion, mood changes, muscle spasm, nausea and vomiting, nephrolithiasis, tremor, weight loss.
What are the side effects of lamotrigine?
Blurred vision, arthralgia, ataxia, diarrhoea, dizziness, headache, insomnia, rash, tremor.
Steven johnson syndrome - Toxic Epidermal Necrolysis or Hypersensitivity syndrome in 1:4000 patients. It is more common in children that adults, more common with co-administration of Valproate, higher doses and rapid titration
What are the side effects of carbamazepine?
Ataxia, blood disorders, blurring of vision, fatigue, hyponatraemia, skin problems
What are the side effects of sodium valproate?
Ataxia, Anaemia, confusion, gastric irritation, haemorrhage, hyponatraemia, tremor, weight gain.
What are the side effects of phenytoin?
Acne, anorexia, constipation, dizziness, gingival hypertrophy, hirsutism, insomnia, rash, tremor.
What is the DVLA guidance for epilepsy?
For car/motorbike licence: reapply after 6 months for a one-off seizure, or after 1 year for more than one seizure. After a seizure following a change in anti-epileptic medications, reapply to drive if the seizure was more than 6 months ago or you’ve been back on the previous medication for 6 months.
For bus/coach/lorry licence: reapply after 5 years for a one-off seizure if no anti-epileptic medications have been taken during this period. For more than one seizure, reapply after 10 seizure-free years during which no anti-epileptic medication has been taken.
Explain the difference between non-epileptic seizures and epileptic seizures?
Non-epileptic seizures can present with features such as pelvic thrusting, head movements during the attack, eyes closed, and prolonged duration (greater than 3 minutes), contrasting with the postictal symptoms of confusion, tongue biting, incontinence, and raised prolactin levels typically observed in epileptic seizures.
What do we give for status epilepticus in hospital vs community
- IV lorazepam (hospital)
- PR diazepam (community)
Which medications are most commonly associated with reducing the seizure threshold?
Ciprofloxacin and other quinolones can precipitate seizures in patients with or without an underlying seizure disorder. They should be prescribed with extreme caution in patients with epilepsy.
Describe juvenile myoclonic seizures?
Juvenile myoclonic epilepsy is usually seen in adolescence. It is commonly seen 1-2 hours after waking up and they can be triggered by a lack of sleep. Myoclonic seizures are often described as shock-like irregular movements of a limb. It will likely need treatment with anti-epileptics but the condition has a high response rate to medications.
When is phenytoin given?
There is evidence for the use of phenytoin within the first 7 d after a traumatic brain injury to prevent early seizures; however, there is insufficient evidence to show a benefit beyond this
Patients with temporal lobe epilepsy may experience hippocampal damage leading to deficits in x?
Long term memory
What is an essential tremor?
Essential tremor (ET) is a chronic neurologic condition that typically manifests as an involuntary shaking or trembling usually on changing posture or performing an action, most commonly in the hands and arms, but can also affect other body parts such as the head, voice, lower limbs, tongue, face, and the trunk.
What causes an essential tremor?
The etiology of ET is complex and not completely understood, but it is believed to be multifactorial, involving both genetic and environmental factors.
In approximately 50% of the cases, ET is inherited as an autosomal dominant trait, suggesting a significant genetic component.
What is the main clinical feature of an essential tremor?
The main clinical feature of ET is a postural or kinetic tremor, which predominantly affects the upper limbs distally.
What are the additional symptoms of essential tremor?
Involvement of the head, lower limbs, voice, tongue, face, and the trunk, although less common.
Increased tremor amplitude over time, causing difficulty with tasks such as writing, eating, holding objects, dressing, and speaking.
Exacerbation of tremor during situations of anxiety, stress, and social interaction.
Potential development of severe psychosocial disability, including depression, particularly in patients with head and voice tremors.
Classically what can improve an essential tremor?
Classically, ingestion of alcohol can temporarily improve the tremor.
What are the investigations for essential tremor?
The diagnosis of ET is mainly clinical.
Once suspected, a thorough evaluation of functional and psychosocial disabilities should be performed using objective scales to determine the need for pharmacotherapy.
Further investigations, such as blood tests or neuroimaging, may be warranted to rule out other potential causes of tremor.
What is the management for essential tremor?
Management of ET is primarily symptomatic and may include:
Pharmacological therapy, using agents such as propranolol (first line), primidone, topiramate, gabapentin, clonazepam.
Surgical intervention for severe cases, including deep brain stimulation, focused ultrasound thalamotomy, and radiosurgical (Gamma Knife) thalamotomy.
If a patient has an essential tremor but suffers from asthma what is the treatment?
Propranolol is contradicted. Other first line pharmacological treatments include topiramate and primidone
Define malaria:
Malaria is a disease caused by protozoan parasites of the Plasmodium genus
Name the different malaria species:
The different malaria species are:
P. falciparum (the most pathogenic species)
P. vivax
P. ovale
P. malariae
P. knowlesi
What is the aetiology for malaria?
The parasitic life cycle of malaria involves a cyclical infection of two hosts: humans and female Anopheles mosquitoes. Infection in humans occurs in two stages: the liver stage and the blood stage. The clinical signs and symptoms of the disease are due to blood-stage parasites and tend to occur at different times depending on the species. Plasmodium falciparum has an incubation period of 7-30 days.
Following the bite of an infected female Anopheles mosquito, parasites, known as sporozoites, are inoculated into the human host, where they transit in the bloodstream to the liver. Sporozoites initially establish infection in hepatocytes, where they replicate and mature into hepatic schizonts. These subsequently rupture and release a form of parasite known as a merozoite into the bloodstream.
Merozoites infect erythrocytes, forming trophozoites that reproduce asexually and mature into blood-stage schizonts, which also rupture, causing the further release of merozoites. Some trophozoites differentiate into male or female gametocytes, which may be ingested by their second host, the Anopheles mosquito, in subsequent blood meals. Gametocytes reproduce within the stomach of the mosquito, where they form oocysts which grow and release sporozoites, which travel to the mosquito’s salivary glands to further perpetuate the cycle of further inoculation into a new human host.
The clinical manifestations of the disease are due to blood-stage parasites, which cause the accumulation of toxic substances and waste during their development in erythrocytes. Lysis of red blood cells results in the releasing these factors and potent inflammatory immune responses. The incubation period until symptoms appear tends to vary between 7 to 30 days.
What are the risk factors for severe disease in malaria?
Pregnancy
Children
Elderly
Complex comorbidities
Immunosuppression
What are the initial symptoms of malaria?
Fevers which may be cyclical, sweats and chills
Headache, malaise, aches & pains
Abdominal pain, nausea & vomiting, diarrhoea
Patients may have splenomegaly, jaundice, hypotension, pallor and reduced urine output
What are the features of severe malaria?
Abnormal behaviour, seizures or altered consciousness suggest cerebral malaria
Parasitaemia >2%, severe anaemia or haemoglobinuria
Hypoglycaemia, metabolic acidosis, hypovolaemia
Temperature >39C
Acute respiratory distress syndrome, disseminated intravascular coagulation or shock
Renal impairment
Hb < 70 g/L
Hypoglycaemia (<2.2 mmol/L)
What are the investigations for malaria?
Thick and thin blood films are the gold-standard method of diagnosing malaria. The thick film identifies the presence of parasites, and the thin film determines the species. If negative, films should be repeated.
Rapid diagnostic tests can also be used but do not replace the need for blood films.
Other important investigations include:
FBC & film, clotting, U&E’s, LFT’s, glucose measurement
Urine dip ± culture
ABG if severe symptoms
Other investigations to consider include blood cultures, stool culture, chest X-ray and lumbar puncture.
What is the first line treatment for uncomplicated falciparum in malaria?
artemisinin-based combination (Artemether with lumefantrine) therapy
Patients will also require supportive care and antipyretics. In severe cases, ICU admission may be indicated.
What is the first line treatment in uncomplicated non-falciparum in malaria?
artemisinin-combination therapy or chloroquine
Patients will also require supportive care and antipyretics. In severe cases, ICU admission may be indicated.
What is the first line treatment in severe falciparum in malaria?
IV artesunate
Patients will also require supportive care and antipyretics. In severe cases, ICU admission may be indicated.
As malaria is a notifiable disease what does one have to do?
Malaria is a notifiable disease and all cases should be reported to the local health protection team in the first instance.
What is malaria prevention advice?
Avoidance of travel - particularly those who are at higher risk of severe infection
Measures to avoid mosquito bites - avoiding exposure at dusk & down, mosquito nets & screens, repellant, loose clothing
Chemoprophylaxis - drugs available include chloroquine, mefloquine and doxycycline, all of which have pro’s and cons and, as such, should be an individualised decision
Education about malaria, its symptoms and seeking medical attention early. Standby emergency medication may be prescribed if the person is far from medical care.
In uncomplicated non-falciparum malaria what treatment do we give to prevent relapses after chloroquine?
Primaquine is the only drug effective against the hypnozoites (dormant liver-stage parasites) of Plasmodium ovale. After treatment of the acute blood-stage infection with chloroquine, starting primaquine is essential to eradicate the liver-stage hypnozoites. Without this treatment, the patient is at risk of future relapses, as P. ovale can remain dormant in the liver and reactivate later.
which malaria prophylaxis agents should be avoided in a patient with epilepsy?
Mefloquine (Lariam) and chloroquine increase the risk of seizures and are therefore contraindicated in those with epilepsy.
Define meningitis:
Meningitis is an inflammation of the meninges, which are composed of three layers: the dura mater, arachnoid mater, and pia mater. This inflammation may arise from both infective and non-infective aetiologies.
What is the epidemiology of meningitis?
Bacterial meningitis, while not the most common form of meningitis, is particularly significant due to its high morbidity and mortality rates.
Viral meningitis, predominantly caused by enteroviruses, is more common but typically less severe. Fungal and parasitic causes are relatively rare, except in immunosuppressed individuals.
Name the infective causes of meningitis:
Bacterial: Streptococcus pneumoniae (most common bacterial cause), Neisseria meningitidis, Haemophilus influenzae, Listeria monocytogenes, among others.
Viral: Enteroviruses are overall most common (Echoviruses, Coxsackie viruses A and B, poliovirus), herpes viruses (HSV2, HSV1), Paramyxovirus, measles and rubella viruses, Varicella Zoster Virus, Arboviruses, Rabies virus.
Fungal: Particularly Cryptococcus neoformans, mainly affecting the immunosuppressed population.
Parasitic: Amoeba (Acanthamoeba), Toxoplasma gondii.
Name the non-infective causes of meningitis:
Non-infective causes of meningitis encompass:
Malignancies such as leukaemia, lymphoma, and other tumours
Chemical meningitis
Certain drugs, including NSAIDs and trimethoprim
Systemic inflammatory diseases such as sarcoidosis, systemic lupus erythematosus, Behcet’s disease.
What are the cardinal features of meningitis?
Headache
Fever
Neck stiffness
Photophobia
Nausea and vomiting
Focal neurology
Seizures
Reduced conscious level
Features of overwhelming sepsis, such as non-blanching petechial rash indicative of impending Disseminated Intravascular Coagulation (DIC).
What is the kernig sign?
Kernig’s sign is a test performed to evaluate the presence of meningeal irritation and stiffness in the hamstrings and lower back. To perform this test, the patient is positioned lying on their back with the hip and knee flexed at 90 degrees. The examiner then attempts to extend the patient’s knee. If the patient experiences pain and resistance to knee extension, especially when attempting to straighten the leg, it is considered a positive Kernig’s sign. This sign suggests meningeal irritation or inflammation.
What is the Brudzinski’s sign?
Brudzinski’s sign is another manoeuvre used to assess for meningeal irritation. This test involves passive neck flexion, where the examiner gently flexes the patient’s neck forward toward the chest while the patient is lying on their back. If the patient involuntarily flexes their hips and knees in response to neck flexion, it is considered a positive Brudzinski’s sign. This involuntary movement indicates irritation of the meninges.
What are the diagnostic investigations for meningitis?
Blood tests: Full Blood Count, Urea and Electrolytes, Clotting, Glucose, PCT
Arterial Blood Gas
Blood cultures
Bacterial throat swab for meningococcus
PCR for meningococcus & pneumococcus
HIV test
Imaging: CT Head if there are signs of raised intracranial pressure (ICP)
Lumbar puncture for Cerebrospinal Fluid (CSF) analysis, once confirmed there are no signs of raised ICP.
What are the CSF findings in meningitis?
What is the findings in cryptococcal meningitis?
may give any of the results, so should be considered as a differential in any HIV or immunocompromised patient. Classically the opening pressure is very high, and this is a poor prognostic sign. If suspected, request cryptococcal antigen or India Ink staining.
What is the management for meningitis?
Empirical antibiotic therapy for suspected bacterial meningitis typically includes 2g of IV ceftriaxone twice daily to ensure CNS penetration, with IV amoxicillin added in patients at age extremes for listeria coverage.
In primary care, IM benzylpenicillin or ceftriaxone should be given while awaiting urgent transfer to hospital, especially if meningococcal disease is suspected.
Dexamethasone should be given if bacterial meningitis is strongly suspected in the absence of a rash
This has been shown to reduce neurological sequelae in bacterial meningitis but not meningococcal meningitis
In cases of suspected viral encephalitis, IV aciclovir should also be administered. For patients allergic to penicillin, alternatives such as chloramphenicol may be used.
It’s important to note that any empirical antibiotic regimen should be adjusted based on culture results when available.
What should close contacts get when a case of meningitis is confirmed?
Close contacts of the patient should receive prophylactic antibiotics. This will be guided by specialists but may be a single dose of oral ciprofloxacin, or rifampicin.
Bacterial meningitis is a notifiable disease and any suspected cases should be reported to the local health protection team.
What are the complications of meningitis?
Septic shock
Disseminated Intravascular Coagulation
Coma
Subdural effusions
Syndrome of inappropriate antidiuretic hormone secretion
Seizures
Delayed complications: Hearing loss, cranial nerve dysfunction, hydrocephalus, intellectual deficits, ataxia, blindness
Death
What are the findings in Cryptococcal meningoencephalitis?
Immunocompromised individuals, particularly those with HIV and low CD4 counts, are at increased risk for cryptococcal meningoencephalitis, characterised by fever, headaches, photophobia, neck stiffness, cranial nerve palsies, and nonspecific neurological signs, with normal or bland CT head scans and LP findings showing raised opening pressure, slightly elevated protein, and lymphocyte predominance.
A lumbar puncture is performed and the findings are consistent with bacterial meningitis.
Blood cultures grow gram-positive rods.
Which of the following is most likely to be the causative organism?
Listeria monocytogenes is a gram-positive rod bacteria that can cause meningitis. It can be contracted from certain foods, such as soft cheeses. Complications during pregnancy include chorioamnionitis and premature labour, and it can also be transmitted through the placenta causing fetal infection. Treatment is with ampicillin +/- an aminoglycoside.
Define migraine?
Migraine is a primary headache disorder characterised by intense episodes of debilitating headaches, usually unilateral and pulsating in nature. Symptoms may be preceded by an ‘aura’ which manifests as visual disturbances or sensory changes. The pain usually lasts from 4-72 hours and can be accompanied by nausea, vomiting, photophobia, and phonophobia.
What causes migraines?
The exact cause of migraines is not fully understood, but it is likely a combination of genetic and environmental factors.
The triggering factors are variable and can include certain foods, changes in weather, stress, hormonal changes, and certain medications such as oral contraceptives.
What are the signs and symptoms of migraines?
Aura (usually visual or sensory symptoms preceding the headache)
Unilateral throbbing headache
Photophobia and phonophobia
Nausea and/or vomiting
What is the International Headache Society criteria for migraine without aura:
What are the investigations for migraines?
Diagnosis is primarily clinical, based on the history and examination.
A headache diary is important to help identify triggers and response to treatment.
If secondary causes of headaches are suspected, further investigations may be warranted, such as neuroimaging (MRI or CT) or blood tests (ESR, CRP for giant cell arteritis).
What is the acute management for migraines?
Avoidance of triggers:
Identify and avoid potential triggers like certain foods, stress, and poor sleep.
Medications for acute attacks:
Triptans (e.g., Sumatriptan) – avoid in patients with ischaemic heart disease as it vasoconstricts
Paracetamol or an NSAID (e.g., Ibuprofen) can be used in combination with triptans.
Anti-emetics (e.g., Metoclopramide)
Special considerations:
Female patients with migraine with aura should avoid the combined oral contraceptive pill due to increased risk of ischaemic stroke.
Prophylaxis for migraines?
Medications:
Propranolol (contraindicated in asthma) - but first line
Topiramate (teratogenic)
Amitriptyline.
Candesartan.
Injections:
Greater Occipital Nerve Block
Botulinum Toxin Injection
Newer treatments:
Rimegepant (per NICE guidance, May 2023):
Used for preventing episodic migraine.
Suitable when at least 3 preventive treatments have failed.
Indicated for adults with 4-15 migraine attacks per month.
Regular use of acute migraine medications (e.g., triptans, NSAIDs) more than 10-15 days per month can lead to medication overuse headache (MOH).
Patients should be counseled on limiting the use of acute treatments to prevent MOH.
If a patient has 2 or more attacks a month resulting in disability for 3 days or more, standard analgesia and triptans are contraindicated or ineffective, or an uncommon form of migraine, prevention should be considered.
How to differentiate between migraines and idiopathic intracranial hypertension?
Idiopathic Intracranial Hypertension can present with headaches that appear similar to migraines but usually have some atypical features, e.g., becoming worse on lying down or with vagal manoeuvres such as coughing or sneezing.
How should sumatriptan be taken for migraines?
Sumatriptan should be taken once the headache starts, but not during the aura phase
What are the different motor neurone disease subtypes and do they cause upper or lower motor neurone disease signs?
Imagine findings in multiple sclerosis:
What is the Mcdonald criteria for multiple sclerosis?
What are clinical features of Erb’s palsy?
- Loss of shoulder abduction and elbow flexion
- Arm held internally rotated
- Waiter’s tip
- What levels of the spinal cord are affected?C5-C6
A map of the investigations for subarachnoid haemorrhages:
Describe how a subdural haemorrhage clot changes on CT over time:
Hyperacute phase (<1 hour): The clot may appear isodense, with underlying cerebral oedema.
Acute phase (<3 days): The clot appears as a crescent-shaped hyperdense extra-axial collection over the affected hemisphere.
Sub-acute phase (3 days to 3 weeks): The clot appears more isodense compared to the adjacent cortex, making identification more difficult. Contrast-enhanced CT or MRI can aid identification. There may be associated mass effect causing midline shift and sulcal effacement.
Chronic phase (>3 weeks): The haematoma appears hypodense relative to the adjacent cortex.
What is the most common classification for stroke?
Bamford/Oxford Stroke Classification System
What is the rule of 4 for cortical strokes?
4 motor syndromes are midline:
- Medial Longitudinal fascicles (eye motor)
-Motor Tract of the UMN (corticospinal tract)
-Medial meniscus (proprioception/vibration)
-Motor nuclei of CN
4 sensory syndromes are side (lateral)
- spinothalamic tract (pain + temp)
- spinocerebellar tract (RAM)
-sympathetic chain (dilation, sweating)
- sensory CN nuclei
Cranial nerve lesions are ipsilateral, except trochlear
