Medicine - Neurology Flashcards

1
Q

What are siezures?

A

. Seizures are transient episodes of abnormal electrical activity in the brain.

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2
Q

What are the types of seizures generally seen in adults?

A

Generalised tonic-clonic seizures
Partial seizures (or focal seizures)
Myoclonic seizures
Tonic seizures
Atonic seizures

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3
Q

What are the common types of seizures seen in children?

A

Absence seizures
Infantile spasms
Febrile convulsions

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4
Q

What are generalised tonic-clonic seizures?

A

Generalised tonic-clonic seizures involve tonic (muscle tensing) and clonic (muscle jerking) movements associated with a complete loss of consciousness. Typically, the tonic phase comes before the clonic phase. There may be tongue biting, incontinence, groaning and irregular breathing

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5
Q

What are tonic clonic seizures also called?

A

grand mal seizures

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6
Q

What might patient experience before a tonic clonic seizure?

A

Before the seizure, patients might experience aura, an abnormal sensation that gives a warning that a seizure will occur

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7
Q

What is a post ictal period

A

After the tonic clonic seizure, there is a prolonged post-ictal period, where the person is confused, tired, and irritable or low.

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8
Q

What are Partial seizures (or focal seizures)

A

Partial seizures (or focal seizures) occur in an isolated brain area, often in the temporal lobes. They affect hearing, speech, memory and emotions.

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9
Q

TRUE or FALSE
Patients remain awake during partial seizures

A

TRUE

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10
Q

In which seizures do you see loss of awareness and in which seizures do they have awareness?

A

They remain aware during simple partial seizures but lose awareness during complex partial seizures

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11
Q

There are various symptoms associated with partial seizures, depending on the location of the abnormal electrical activity:

A
  • Déjà vu
  • Strange smells, tastes, sight or sound sensations
  • Unusual emotions
  • Abnormal behaviours
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12
Q

What are myoclonic seizures?

A

Myoclonic seizures present with sudden, brief muscle contractions, like an abrupt jump or jolt. They remain awake. Myoclonic seizures can occur as part of juvenile myoclonic epilepsy in children.

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13
Q

What are tonic seizures?

A

Tonic seizures involve a sudden onset of increased muscle tone, where the entire body stiffens. This results in a fall if the patient is standing, usually backwards. They last only a few seconds, or at most a few minutes.

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14
Q

What are Atonic seizures

A

Atonic seizures (causing “drop attacks”) involve a** sudden loss of muscle tone,** often resulting in a fall. They last only briefly, and patients are usually aware during the episodes. They often begin in childhood. They may be indicative of Lennox-Gastaut syndrome.

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15
Q

What are Absence seizures

A

Absence seizures are usually seen 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 do not respond. These typically last 10 to 20 seconds. Most patients stop having absence seizures as they get older.

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16
Q

Infantile spasms are also known as

A

West syndrome

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17
Q

What is Infantile spasms

A

It is a rare (1 in 4,000) disorder starting at around six months of age. It presents with clusters of full-body spasms. Hypsarrhythmia is the characteristic EEG finding. It is associated with developmental regression and has a poor prognosis.

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18
Q

Tx for Infantile spasms

A

Treatment is with ACTH and vigabatrin.

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19
Q

What are Febrile convulsions

A

Febrile convulsions are tonic-clonic seizures that occur in children during a high fever. They are not caused by epilepsy or other pathology (e.g., meningitis or tumours). Febrile convulsions occur in children aged between 6 months and 5 years. Febrile convulsions do not usually cause any lasting damage. One in three will have another febrile convulsion. They slightly increase the risk of developing epilepsy.

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20
Q

It is essential to differentiate seizures from other conditions with a similar presentation, such as:

A
  • Vasovagal syncope (fainting)
  • Pseudoseizures (non-epileptic attacks)
  • Cardiac syncope (e.g., arrhythmias or structural heart disease)
  • Hypoglycaemia
  • Hemiplegic migraine
  • Transient ischaemic attack
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21
Q

What Ix are done is epilepsy and what do they show?

A

Electroencephalogram (EEG) shows typical patterns in different forms of epilepsy and supports the diagnosis.

MRI brain is used to diagnose structural pathology (e.g., tumours).

Additional investigations can be considered to exclude associated pathology:

  • ECG
  • Serum electrolytes, including sodium, potassium, calcium and magnesium
  • Blood glucose for hypoglycaemia and diabetes
  • Blood cultures, urine cultures and lumbar puncture where sepsis, encephalitis or meningitis is suspected
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22
Q

Patients and families presenting with seizures are advised about safety precautions and recognising, managing and reporting further seizures. Safety precautions include:

A

The DVLA will remove their driving licence until specific criteria are met (e.g., being seizure-free for one year)
Taking showers rather than baths (drowning is a major risk in epilepsy)
Particular caution with swimming, heights, traffic and dangerous equipment

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23
Q

Mx

A
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24
Q

Mx

A
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25
Q

How does sodium valproate work?

A

Sodium valproate works by increasing the activity of gamma-aminobutyric acid (GABA), which has a calming effect on the brain.

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26
Q

What are notable side effects of sodium Valproate?

A

Teratogenic (harmful in pregnancy)
Liver damage and hepatitis
Hair loss
Tremor
Reduce fertility

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27
Q

Sodium valproate in pregnancy can cause ________ _______ _______ and ________________ _____

A

Sodium valproate in pregnancy can cause neural tube defects and developmental delay

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28
Q

There are strict rules for avoiding sodium valproate in females with childbearing potential unless there are no suitable alternatives and strict criteria are met. The __________ __________ __________ __________ is in place to ensure this happens, which involves ensuring effective contraception and an annual risk acknowledgement form.

A

There are strict rules for avoiding sodium valproate in females with childbearing potential unless there are no suitable alternatives and strict criteria are met. The Valproate Pregnancy Prevention Programme is in place to ensure this happens, which involves ensuring effective contraception and an annual risk acknowledgement form.

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29
Q

What is Status Epilepticus

A

Status epilepticus is a medical emergency defined as either:

  • A seizure lasting more than 5 minutes
  • Multiple seizures without regaining consciousness in the interim
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30
Q

Management for Status Epilepticus

A

Management of status epilepticus involves an ABCDE approach, including:

  • Securing the airway
  • Giving high-concentration oxygen
  • Checking blood glucose levels
  • Gaining intravenous access (inserting a cannula)

Medical treatment involves:

  • A benzodiazepine first-line, repeated after 5-10 minutes if the seizure continues
  • Second-line options (after two doses of benzodiazepine) are IV levetiracetam, phenytoin or sodium valproate
  • Third-line options are phenobarbital or general anaesthesia
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31
Q

Status Epilepticus
Options for benzodiazepines?

A
  • Buccal midazolam (10mg)
  • Rectal diazepam (10mg)
  • Intravenous lorazepam (4mg)
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32
Q

What is Guillain-Barre syndrome?

A

Guillain-Barré syndrome is an acute paralytic polyneuropathy that affects the peripheral nervous system. It causes acute, symmetrical, ascending weakness and can also cause sensory symptoms. It is usually triggered by an infection

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33
Q

Guillain-Barré is particularly associated with?

A

Campylobacter jejuni, cytomegalovirus (CMV) and Epstein-Barr virus (EBV)

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34
Q

What is the patho of Guillain-Barré

A

Guillain-Barré is thought to occur due to a process called molecular mimicry. The B cells of the immune system create antibodies against the antigens on the triggering pathogen. These antibodies also match proteins on the peripheral neurones. They may target proteins on the myelin sheath or the nerve axon itself.

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35
Q

What is the presentation of Guillain-Barré

A

Symptoms usually start within four weeks of the triggering infection. They begin in the feet and progress upward. Symptoms peak within 2-4 weeks. Then, there is a recovery period that can last months to years.

The characteristic features are:

  • Symmetrical ascending weakness
  • Reduced reflexes

There may be peripheral loss of sensation or neuropathic pain. It may progress to the cranial nerves and cause facial weakness. Autonomic dysfunction can lead to urinary retention, ileus or heart arrhythmias.

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36
Q

Diagnosis of Guillain-Barré

A

The diagnosis of Guillain-Barré syndrome is made clinically (using the Brighton criteria), supported by investigations:

  • Nerve conduction studies (showing reduced signal through the nerves)
  • Lumbar puncture for cerebrospinal fluid (showing raised protein with a normal cell count and glucose)
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37
Q

Management of Guillain-Barré

A

Management involves:

  • Supportive care
  • VTE prophylaxis (pulmonary embolism is a leading cause of death)
  • IV immunoglobulins (IVIG) first-line
  • Plasmapheresis is an alternative to IVIG

Severe cases with respiratory failure may require intubation, ventilation and admission to the intensive care unit.

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38
Q

Prognosis of Guillain-Barré

A

Recovery can take months to years. Patients can continue regaining function five years after the acute illness. Most patients eventually make either a full recovery or are left with minor symptoms. Some are left with significant disability. Mortality is around 5%, mainly due to respiratory or cardiovascular complications.

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39
Q

Intracranial haemorrhage refers to bleeding within the skull. There are four types: What are they?

A
  • Extradural haemorrhage (bleeding between the skull and dura mater)
  • Subdural haemorrhage (bleeding between the dura mater and arachnoid mater)
  • Intracerebral haemorrhage (bleeding into brain tissue)
  • Subarachnoid haemorrhage (bleeding in the subarachnoid space)
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40
Q
A
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41
Q

____________ haemorrhage and ____________ haemorrhage account for 10-20% of strokes.

A

Intracerebral haemorrhage and subarachnoid haemorrhage account for 10-20% of strokes.

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42
Q

Risk factors for Intracranial Bleeds

A
  • Head injuries
  • Hypertension
  • Aneurysms
  • Ischaemic strokes (progressing to bleeding)
  • Brain tumours
  • Thrombocytopenia (low platelets)
  • Bleeding disorders (e.g., haemophilia)
  • Anticoagulants (e.g., DOACs or warfarin)
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43
Q

Presentation of Intracranial Bleeds

A

Sudden-onset headache is a key feature. They can also present with:

  • Seizures
  • Vomiting
  • Reduced consciousness
  • Focal neurological symptoms (e.g., weakness)
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44
Q

What is the Glasgow Coma Scale

A

The Glasgow Coma Scale (GCS) is a universal assessment tool for the level of consciousness. It is scored based on eyes, verbal response and motor response. The maximum score is 15/15, and the minimum is 3/15. A score of 8/15 needs airway support, as there is a risk of airway obstruction or aspiration, leading to hypoxia and brain injury

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45
Q

Extradural haemorrhage occurs between the ____ and ____ mater and is usually caused by a rupture of the ________ ________ ________ in the ____________ region

A

Extradural haemorrhage occurs between the skull and dura mater and is usually caused by a rupture of the middle meningeal artery in the temporoparietal region

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46
Q

What fracture is associated with Extradural Haemorrhage

A

fracture of the temporal bone

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47
Q

What would you see in CT for extradural haemorrhage

A

On a CT scan, they have a bi-convex shape and are limited by the cranial sutures (they do not cross the sutures, which are the points where the skull bones join together).

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48
Q

What is a typical history of extradural haemorrhage?

A

A typical history is a young patient with a traumatic head injury and an ongoing headache. They have a period of improved neurological symptoms and consciousness, followed by a rapid decline over hours as the haematoma gets large enough to compress the intracranial contents.

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49
Q

Subdural haemorrhage occurs between the _____ _____ and __________ ______ and is caused by a rupture of the ________ ____ in the outermost meningeal layer.

A

Subdural haemorrhage occurs between the dura mater and arachnoid mater and is caused by a rupture of the bridging veins in the outermost meningeal layer.

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50
Q

What does a subdural harmorrhage show on CT scan

A

On a CT scan, they have a crescent shape and are not limited by the cranial sutures (they can cross over the sutures).

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51
Q

Typical history of subdural haemorrhage?

A

Subdural haemorrhages may occur in elderly and alcoholic patients, who have more atrophy in their brains, making the vessels more prone to rupture.

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52
Q

What is Intracerebral Haemorrhage

A

Intracerebral haemorrhage involves bleeding in the brain tissue. It presents similarly to an ischaemic stroke with sudden-onset focal neurological symptoms, such as limb or facial weakness, dysphasia or vision loss.

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53
Q

Intracerebral Haemorrhage can occur spontaneously or secondary to __________ ______, ________ or ___________ _______.

A

They can occur spontaneously or secondary to **ischaemic stroke, tumours or aneurysm rupture.

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54
Q

What is Subarachnoid Haemorrhage

A

Subarachnoid haemorrhage involves bleeding in the subarachnoid space, where the cerebrospinal fluid is located, between the pia mater and the arachnoid membrane. This is usually the result of a ruptured **cerebral aneurysm. **

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55
Q

What is the typical history of Subarachnoid Haemorrhage

A

The typical history is a sudden-onset occipital headache during strenuous activity, such as heavy lifting or sex. The sudden and severe onset leads to the “thunderclap headache” description.

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56
Q

Diagnosis of Intracranial Bleeds

A

Immediate imaging (e.g., CT head) is required to establish the diagnosis. Bloods should include a full blood count (for platelets) and a **coagulation screen. **

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57
Q

What is initial management of Intracranial Bleeds

A
  • Admission to a specialist stroke centre
  • Discuss with a specialist neurosurgical centre to consider surgical treatment
  • Consider intubation, ventilation and intensive care if they have reduced consciousness
  • Correct any **clotting abnormality **(e.g., platelet transfusions or vitamin K for warfarin)
  • Correct severe hypertension but avoid hypotension
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58
Q

Intracranial Bleeds
Smaller bleeds may be managed conservatively with close monitoring and ______ ______

A

Smaller bleeds may be managed conservatively with close monitoring and repeat imaging.

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59
Q

Surgical options for treating an extradural or subdural haematoma are:

A
  • Craniotomy (open surgery by removing a section of the skull)
  • Burr holes (small holes drilled in the skull to drain the blood)
    *
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60
Q

Brain tumours range from benign (e.g., ____________) to highly malignant (e.g., ____________).

A

Brain tumours range from benign (e.g., meningiomas) to highly malignant (e.g., glioblastomas).

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61
Q

Brain tumours may be asymptomatic, particularly when they are small. As they grow, they present with ____________ ______ __________ symptoms depending on the location of the lesion.

A

Brain tumours may be asymptomatic, particularly when they are small. As they grow, they present with **progressive focal neurological **symptoms depending on the location of the lesion.

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62
Q

Brain tumours often present with symptoms and signs of …

A

Brain tumours often present with symptoms and signs of raised intracranial pressure (intracranial hypertension).

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63
Q

What is a common presentation for frontal lobe tumour?

A

A common exam scenario is an unusual change in personality and behaviour, which indicates a frontal lobe tumour. The frontal lobe is responsible for personality and higher-level decision-making.

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64
Q

The causes of increased pressure in the intracranial space include:

A
  • Brain tumours
  • Intracranial haemorrhage
  • Idiopathic intracranial hypertension
  • Abscesses or infection
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65
Q

In patients presenting with headaches, the concerning features that may indicate intracranial hypertension include:

A
  • Constant headache
  • Nocturnal (occurring at night)
  • Worse on waking
  • Worse on coughing, straining or bending forward
  • Vomiting
  • Papilloedema on fundoscopy
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66
Q

Other presenting features of raised intracranial hypertension may include:

A
  • Altered mental state
  • Visual field defects
  • Seizures (particularly partial seizures)
  • Unilateral ptosis (drooping upper eyelid)
  • Third and sixth nerve palsies
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67
Q

What is papiloedema?

A

Papilloedema is a crucial fundoscopy finding in patients with increased intracranial pressure. Papilloedema describes swelling of the optic disc secondary to raised intracranial pressure. Papill- refers to a small, rounded, raised area (the optic disc) and -oedema refers to the swelling.

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68
Q

Patho of papilloedema?

A

The sheath around the optic nerve is connected with the subarachnoid space. The raised cerebrospinal fluid (CSF) pressure flows into the optic nerve sheath, increasing the pressure around the optic nerve behind the optic disc causing the optic disc to bulge forward.

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69
Q

Papilloedema can be seen on fundoscopy as:

A
  • Blurring of the optic disc margin
  • Elevated optic disc (look for the way the retinal vessels flow across the disc to see the elevation)
  • Loss of venous pulsation
  • Engorged retinal veins
  • Haemorrhages around the optic disc
  • Paton’s lines, which are creases or folds in the retina around the optic disc
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70
Q

What is Gliomas

A

Gliomas are tumours of the glial cells in the brain or spinal cord. Glial cells surround and support the neurones. Glial cells include astrocytes, oligodendrocytes and ependymal cells.

71
Q

How does the grading work in gliomas?

A

Gliomas are graded from 1 to 4. Grade 1 is the most benign (possibly curable with surgery), and grade 4 is the most malignant (e.g., glioblastoma multiforme)

72
Q

What is the three main types of gilomas

A

The main three types (roughly from most to least malignant) are:

  • Astrocytoma (the most common and aggressive form is glioblastoma)
  • Oligodendroglioma
  • Ependymoma
73
Q

What are Meningiomas

A

Meningiomas are tumours growing from the cells of the meninges. They are usually benign. However, they take up space, and this “mass effect” can lead to raised intracranial pressure and neurological symptoms.

74
Q

The cancers that most often spread to the brain are:

A

Lung
Breast
Renal cell carcinoma
Melanoma

75
Q

What visual defect does pituitary tumours cause?

A

Pituitary tumours tend to be benign. If they grow large enough, they can press on the optic chiasm, causing a visual field defect called bitemporal hemianopia, with loss of the outer half of the visual fields in both eyes.

76
Q

They can cause hormone deficiencies (hypopituitarism) or to release excessive hormones, leading to:

A
  • Acromegaly (excessive growth hormone)
  • Hyperprolactinaemia (excessive prolactin)
  • Cushing’s disease (excessive ACTH and cortisol)
  • Thyrotoxicosis (excessive TSH and thyroid hormone)
77
Q

Pituitary tumours may be managed with:

A
  • Trans-sphenoidal surgery (through the nose and sphenoid bone)
  • Radiotherapy
  • Bromocriptine to block excess prolactin
  • Somatostatin analogues (e.g., octreotide) to block excess growth hormone
78
Q

What are Acoustic Neuromas

A

Acoustic neuromas are benign tumours of the Schwann cells that surround the auditory nerve (vestibulocochlear nerve) that innervates the inner ear. Schwann cells provide the myelin sheath around neurones of the peripheral nervous system. Acoustic neuromas are also called vestibular schwannomas.

79
Q

Where do Acoustic Neuromas occur

A

They occur at the cerebellopontine angle and are sometimes called **cerebellopontine angle tumours. **

80
Q

Are acoustic neuromas normally bilateral or unilateral?

A

They are usually unilateral. Bilateral acoustic neuromas are associated with neurofibromatosis type 2.

81
Q

Acoustic Neuroma
The typical patient is a 40-60 year old presenting with a gradual onset of:

A
  • Unilateral sensorineural hearing loss (often the first symptom)
  • Unilateral tinnitus
  • Dizziness or imbalance
  • Sensation of fullness in the ear
  • Facial nerve palsy (if the tumour grows large enough to compress the facial nerve
82
Q

Acoustic Neuroma Management options

A

Management options include:

  • Conservative management with monitoring may be used if there are no symptoms or treatment is inappropriate
  • Surgery to remove the tumour (partial or total removal)
  • Radiotherapy to reduce the growth
83
Q

Management of brain tumours

A

MRI scan is the first-line investigation in patients with a possible brain tumour.

Biopsy gives the definitive histological diagnosis, usually obtained during surgery to remove the tumour.

The management of brain tumours depends on the type and grade, guided by the multidisciplinary team. The main options are:

  • Surgery
  • Chemotherapy
  • Radiotherapy
  • Palliative care
84
Q

What is Subarachnoid haemorrhage

A

Subarachnoid haemorrhage involves bleeding in the subarachnoid space, where the **cerebrospinal fluid **is located, between the pia mater and the arachnoid membrane. This is usually the result of a ruptured cerebral aneurysm.

85
Q

Subarachnoid haemorrhage has a very high ________ (around 30%) and ____________, making it essential not to miss.

A

Subarachnoid haemorrhage has a very high mortality (around 30%) and morbidity, making it essential not to miss.

86
Q

Risk Factors for subarachnoid haemorrhage

A

It is more common in:

  • Aged 45 to 70
  • Women
  • Black ethnic origin

General risk factors include:

  • Hypertension
  • Smoking
  • Excessive alcohol intake
87
Q

Subarachnoid haemorrhage is particularly associated with:

A
  • Family history
  • Cocaine use
  • Sickle cell anaemia
  • Connective tissue disorders (e.g., Marfan syndrome or Ehlers-Danlos syndrome)
  • Neurofibromatosis
  • Autosomal dominant polycystic kidney diseas
88
Q

Presentation of subarachnoid haemorrhage

A

The typical history is a sudden-onset occipital headache during strenuous activity, such as heavy lifting or sex. The sudden and severe onset leads to the** “thunderclap headache”** description. It may feel like being struck over the back of the head.

Other important features include:

* Neck stiffness
* Photophobia
* Vomiting
* Neurological symptoms (e.g., visual changes, dysphasia, focal weakness, seizures and reduced consciousness)

89
Q

Investigations for subarachnoid Haemorrhage?

A

CT head is the first-line investigation. Blood will cause hyper-attenuation in the subarachnoid space. However, a normal CT head does not exclude a subarachnoid haemorrhage. CT is less reliable more than 6 hours after the start of symptoms.

Lumbar puncture is considered after a normal CT head. The NICE guidelines (2022) recommend waiting at least 12 hours after the symptoms start before performing a lumbar puncture, as it takes time for the bilirubin to accumulate in the cerebrospinal fluid (CSF). With a subarachnoid haemorrhage, a CSF sample will show:

  • Raised red cell count (a decreasing red cell count on successive bottles may be due to a traumatic procedure)
  • Xanthochromia (a yellow colour to the CSF caused by bilirubin)

CT angiography is used after confirming the diagnosis to locate the source of the bleeding

90
Q

Management of subarachnoid Haemorrhage>

A

Patients should be managed by a specialist neurosurgical unit. Patients with reduced consciousness may require intubation and ventilation. Supportive care involves a multi-disciplinary team during the initial stages and recovery.

Surgical intervention may be used to treat aneurysms. The aim is to repair the vessel and prevent re-bleeding. This can be done by** endovascular coiling**, which involves inserting a catheter into the arterial system (an endovascular approach), placing platinum coils in the aneurysm and sealing it off from the artery. An alternative is neurosurgical clipping, which involves cranial surgery and putting a clip on the aneurysm to seal it.

91
Q

____________ is a calcium channel blocker used to prevent vasospasm. Vasospasm is a common complication following a subarachnoid haemorrhage, resulting in brain ischaemia.

A

Nimodipine is a calcium channel blocker used to prevent vasospasm. Vasospasm is a common complication following a subarachnoid haemorrhage, resulting in brain ischaemia.

92
Q

____________ refers to increased cerebrospinal fluid, causing expansion of the ventricles.

A

Hydrocephalus refers to increased cerebrospinal fluid, causing expansion of the ventricles.

93
Q

Hydrocephalus refers to increased cerebrospinal fluid, causing expansion of the ventricles. Treatment options include:

A
  • Lumbar puncture
  • External ventricular drain (a drain inserted into the brain ventricles to drain CSF)
  • Ventriculoperitoneal (VP) shunt (a catheter connecting the ventricles with the peritoneal cavity)
94
Q

What is Multiple sclerosis (MS)

A

Multiple sclerosis (MS) is a chronic and progressive autoimmune condition involving demyelination in the central nervous system. The immune system attacks the myelin sheath of the myelinated neurones.

95
Q

Multiple sclerosis typically presents in young adults (under ____ years) and is more common in ________.

A

Multiple sclerosis typically presents in young adults (under 50 years) and is more common in women.

96
Q

Myelin covers the axons of neurones and helps electrical impulses travel faster. Myelin is provided by cells that wrap themselves around the axons:

A

Oligodendrocytes in the central nervous system

Schwann cells in the peripheral nervous system

97
Q

Multiple sclerosis affects the central nervous system (the ____________). Inflammation and immune cell infiltration cause damage to the myelin, affecting the electrical signals moving along the neurones.

A

Multiple sclerosis affects the central nervous system (the oligodendrocytes). Inflammation and immune cell infiltration cause damage to the myelin, affecting the electrical signals moving along the neurones.

98
Q

A characteristic feature of MS is that lesions vary in location, meaning that the affected sites and symptoms change over time. The lesions are described as….

A

A characteristic feature of MS is that lesions vary in location, meaning that the affected sites and symptoms change over time. The lesions are described as “disseminated in time and space”.

99
Q

The cause of the multiple sclerosis is unclear, but there is growing evidence that it may be influenced by

A

Multiple genes
Epstein–Barr virus (EBV)
Low vitamin D
Smoking
Obesity

100
Q

Onset of MS

A

Symptoms usually progress over more than 24 hours. Symptoms tend to last days to weeks at the first presentation and then improve. There are many ways MS can present, depending on the location of the lesions.

101
Q

What is the most common presentation of multiple sclerosis.

A

Optic neuritis is the most common presentation of multiple sclerosis. It involves demyelination of the optic nerve and presents with unilateral reduced vision, developing over hours to days

102
Q

Key features of optic neuritis are:

A
  • Central scotoma (an enlarged central blind spot)
  • Pain with eye movement
  • Impaired colour vision
  • Relative afferent pupillary defect
103
Q

Other causes of optic neuritis include

A

Sarcoidosis
Systemic lupus erythematosus
Syphilis
Measles or mumps
Neuromyelitis optica
Lyme disease

104
Q

Patients presenting with acute loss of vision need urgent ophthalmology input. Optic neuritis is treated with

A

Patients presenting with acute loss of vision need urgent ophthalmology input. Optic neuritis is treated with high-dose steroids

105
Q

Lesions affecting the oculomotor (CN III), trochlear (CN IV) or abducens (CN VI) can cause …..

A

double vision (diplopia) and nystagmus

106
Q

What do Oscillopsia refer to?

A

Oscillopsia refers to the visual sensation of the environment moving and being unable to create a stable image

107
Q

Internuclear ophthalmoplegia is caused by a lesion in the

A

medial longitudinal fasciculus.

108
Q

The nerve fibres of the medial longitudinal fasciculus connect the ________ ______ ______ (“internuclear”) that control eye movements (the 3rd, 4th and 6th cranial nerve nuclei). These fibres are responsible for coordinating the eye movements to ensure the eyes move together. It causes impaired ________ on the same side as the lesion (the ipsilateral eye) and ________ in the contralateral abducting eye.

A

The nerve fibres of the medial longitudinal fasciculus connect the cranial nerve nuclei (“internuclear”) that control eye movements (the 3rd, 4th and 6th cranial nerve nuclei). These fibres are responsible for coordinating the eye movements to ensure the eyes move together. It causes impaired** adduction** on the same side as the lesion (the ipsilateral eye) and nystagmus in the contralateral abducting eye.

109
Q

A lesion in the ________ causes a conjugate lateral gaze disorder

A

A lesion in the abducens (CN VI) causes a conjugate lateral gaze disorder

110
Q

What is conjugate lateral gaze disorder

A

Conjugate means connected. Lateral gaze is where both eyes move to look laterally to the left or right. When looking laterally in the direction of the affected eye, the affected eye will not be able to abduct. For example, in a lesion involving the left eye, when looking to the left, the right eye will adduct (move towards the nose), and the left eye will remain in the middle.

111
Q

Multiple sclerosis may present with focal weakness, for example:

A

Incontinence
Horner syndrome
Facial nerve palsy
Limb paralysis

112
Q

Multiple sclerosis may present with focal sensory symptoms, for example:

A

Trigeminal neuralgia
Numbness
Paraesthesia (pins and needles)
Lhermitte’s sign

113
Q

What is Lhermitte’s sign

A

Lhermitte’s sign describes an electric shock sensation that travels down the spine and into the limbs when flexing the neck. It indicates disease in the cervical spinal cord in the dorsal column. It is caused by stretching the demyelinated dorsal column.

114
Q

What is transverse myelitis

A

Transverse myelitis refers to a site of inflammation in the spinal cord, which results in sensory and motor symptoms depending on the location of the lesion.

115
Q

What is Ataxia

A

Ataxia is a problem with coordinated movement. It can be sensory or cerebellar.

116
Q

Sensory ataxia is due to loss of ________ which is the ability to sense the position of the joint (e.g., is the joint flexed or extended).

A

Sensory ataxia is due to loss of proprioception, which is the ability to sense the position of the joint (e.g., is the joint flexed or extended).

117
Q

A lesion in the ______ __________ of the spine can cause sensory ataxia.

A

A lesion in the dorsal columns of the spine can cause sensory ataxia.

118
Q

What is present in sensory ataxia

A

This results in a positive Romberg’s test (they lose balance when standing with their eyes closed) and can cause pseudoathetosis (involuntary writhing movements)

119
Q

What is Cerebellar ataxia

A

Cerebellar ataxia results from problems with the cerebellum coordinating movement, indicating a cerebellar lesion.

120
Q

What is Clinically isolated syndrome

A

Clinically isolated syndrome describes the first episode of demyelination and neurological signs and symptoms. Patients with clinically isolated syndrome may never have another episode or may go on to develop MS. Lesions on an MRI scan suggest they are more likely to progress to MS.

121
Q

What is Relapsing-remitting MS

A

Relapsing-remitting MS is the most common pattern when first diagnosed. It is characterised by episodes of disease and neurological symptoms followed by recovery. The symptoms tend to occur in different areas with each episode. I

122
Q

Relapsing-remitting MS can be further classified based on whether the disease is active or worsening:

A
  • Active: new symptoms are developing, or new lesions are appearing on the MRI
  • Not active: no new symptoms or MRI lesions are developing
  • Worsening: there is an overall worsening of disability over time
  • Not worsening: there is no worsening of disability over time
123
Q

What is Secondary progressive MS

A

Secondary progressive MS is where there was relapsing-remitting disease, but now there is a progressive worsening of symptoms with incomplete remissions. Symptoms become increasingly permanent. Secondary progressive MS can be further classified based on whether the disease is active or progressing.

124
Q

What is Primary progressive MS

A

Primary progressive MS involves worsening disease and neurological symptoms from the point of diagnosis without relapses and remissions. This can be further classified based on whether it is active or progressing.

125
Q

MS
The diagnosis is made by a neurologist based on the clinical picture and symptoms suggesting lesions that change location over time. Other causes for the symptoms need to be excluded.

Investigations can support the diagnosis:

A
  • MRI scans can demonstrate typical lesions
  • Lumbar puncture can detect oligoclonal bands in the cerebrospinal fluid (CSF)
126
Q

MS relapse management

A

Relapses may be treated with steroids. The NICE guidelines (2022) suggest either:

  • 500mg orally daily for 5 days
  • 1g intravenously daily for 3–5 days (where oral treatment has previously failed or where relapses are severe)
127
Q
A
128
Q
A
128
Q

Symptomatic treatments for MS include:

A
  • Exercise to maintain activity and strength
  • Fatigue may be managed with amantadine, modafinil or SSRIs
  • Neuropathic pain may be managed with medication (e.g., amitriptyline or gabapentin)
  • Depression may be managed with antidepressants, such as SSRIs
  • Urge incontinence may be managed with antimuscarinic medications (e.g., solifenacin)
  • Spasticity may be managed with baclofen or gabapentin
  • Oscillopsia may be managed with gabapentin or memantine
129
Q

What is Parkinson’s disease

A

Parkinson’s disease is a condition where there is a progressive reduction in dopamine in the basal ganglia, leading to disorders of movement. The symptoms are characteristically asymmetrical, with one side of the body affected more. The typical patient is an older man, around 70 years old, with a gradual onset of symptoms.

130
Q

There is a classic triad of features in Parkinson’s disease:

A
  • Resting tremor (a tremor that is worse at rest)
  • Rigidity (resisting passive movement)
  • Bradykinesia (slowness of movement)
131
Q

Patho of Parkinson’s

A

The basal ganglia are a group of structures situated near the centre of the brain. They are responsible for coordinating habitual movements such as walking, controlling voluntary movements and learning specific movement patterns.

Dopamine plays an essential role in the basal ganglia function. Patients with Parkinson’s disease have a slow but progressive drop in dopamine production.

132
Q

How is tremor presented in Parkinson’s Disease

A

Tremor in Parkinsons is worse on one side and has a 4-6 hertz frequency, meaning it cycles 4-6 times per second. It is described as a “pill-rolling tremor” due to the appearance of rolling a pill between their fingertips and thumb. It is more noticeable when resting and improves on voluntary movement. It gets worse when the patient is distracted. Performing a task with the other hand (e.g., miming the act of painting a fence) exaggerates the tremor.

133
Q

How is rigidity presented in Parkinson’s Disease

A

Rigidity is resistance to the passive movement of a joint. Taking a hand and passively flexing and extending the arm at the elbow demonstrates tension in the arm that gives way to movement in small increments (like little jerks). The jerking resistance to movement is described as “cogwheel” rigidity.

134
Q

How is Bradykinesia presented in Parkinson’s Disease

A

Bradykinesia describes the movements getting slower and smaller and presents in several ways:

  • Handwriting gets smaller and smaller (micrographia)
  • Small steps when walking (**“shuffling” gait)
  • Rapid frequency of steps to compensate for the small steps and avoid falling (“festinating” gait)
  • Difficulty initiating movement (e.g., going from standing still to walking)
  • Difficulty in turning around when standing and having to take lots of little steps to turn
  • Reduced facial movements and facial expressions (hypomimia)
135
Q

What are the other features of parkinson’s disease

A
  • Depression
  • Sleep disturbance and insomnia
  • Loss of the sense of smell (anosmia)
  • Postural instability (increasing the risk of falls)
  • Cognitive impairment and memory problems
136
Q

What are the differences between Parkinson’s Diseas and Benign Essential Tremor

A
137
Q

Examples of Parkinson’s-Plus Syndromes

A
  • Parkinson’s-Plus Syndromes
  • Dementia with Lewy bodies
  • Progressive supranuclear palsy
  • Corticobasal degeneration
138
Q

What is Multiple system atrophy

A

Multiple system atrophy is a rare condition where the neurones of various systems in the brain degenerate, including the basal ganglia. The degeneration of the basal ganglia leads to a Parkinson’s presentation. Degeneration in other areas leads to autonomic dysfunction (causing postural hypotension, constipation, abnormal sweating and sexual dysfunction) and cerebellar dysfunction (causing ataxia).

139
Q

Diagnosis
Parkinson’s disease

A

Parkinson’s disease is diagnosed clinically based on the history and examination findings. The diagnosis should be made by an experienced specialist. The NICE guidelines (2017) recommend the** UK Parkinson’s Disease Society Brain Bank Clinical Diagnostic Criteria**.

140
Q

What are the management options for Parkinson’s disease

A

Treatment is initiated and guided by a specialist, tailored to each individual and their response to different medications. There is no cure. Treatment is focused on controlling symptoms and minimising side effects. Patients may describe themselves as “on” when the medications are acting, and they are moving freely, and “off” when the medications wear out, they are experiencing symptoms and their next dose is due.

The treatment options are:

  • Levodopa (combined with peripheral decarboxylase inhibitors)
  • COMT inhibitors
  • Dopamine agonists
  • Monoamine oxidase-B inhibitors
141
Q

Levodopa is _________ _________ taken orally. It is usually combined with a __________ ________ __________ (e.g., carbidopa and benserazide), which stops it from being metabolised in the body before it reaches the brain. Levodopa is the most effective treatment for symptoms but becomes less effective over time. It is often reserved for when other treatments are not controlling symptoms.

A

Levodopa is synthetic dopamine taken orally. It is usually combined with a peripheral decarboxylase inhibitor (e.g., carbidopa and benserazide), which stops it from being metabolised in the body before it reaches the brain. Levodopa is the most effective treatment for symptoms but becomes less effective over time. It is often reserved for when other treatments are not controlling symptoms.

142
Q

Levodopa Combination drugs are

A
  • Co-beneldopa (levodopa and benserazide), with the trade name Madopa
  • Co-careldopa (levodopa and carbidopa), with the trade name Sinemet
143
Q

What is the main effect of levodopa

A

dyskinesia.

144
Q

Dyskinesia refers to abnormal movements associated with excessive motor activity. Examples are:

A
  • Dystonia (where excessive muscle contraction leads to abnormal postures or exaggerated movements)
  • Chorea (abnormal involuntary movements that can be jerking and random)
  • Athetosis (involuntary twisting or writhing movements, usually in the fingers, hands or feet)
145
Q

What is used to manage dyskinesia associated with levodopa.

A

Amantadine which is a glutamate antagonist

146
Q

________ is taken with levodopa (and a decarboxylase inhibitor) to slow the breakdown of the levodopa in the brain. It extends the effective duration of the levodopa.

A

Entacapone is taken with levodopa (and a decarboxylase inhibitor) to slow the breakdown of the levodopa in the brain. It extends the effective duration of the levodopa.

147
Q

Examples of dopamine agonists

A

Bromocriptine
Pergolide
Cabergoline

148
Q

When would you use dopamine agonists for parkinson’s disease

A

They are typically used to delay the use of levodopa, then used in combination with levodopa to reduce the required dose

149
Q

What is a notable side effect of prolonged use of Dopamine agonists

A

Pulmonary fibrosis

150
Q

Examples of Monoamine oxidase-B inhibitors

A
  • Selegiline
  • Rasagiline
151
Q

When would you use Monoamine oxidase-B inhibitors for parkinson’s disease

A

They are typically used to delay the use of levodopa, then in combination with levodopa to reduce the “end of dose” worsening of symptoms.

152
Q

Stroke is also called

A

cerebrovascular accident

153
Q

Cerebrovascular accidents are either:

A
  • Ischaemia or infarction of the brain tissue secondary to a disrupted blood supply (ischaemic stroke)
  • Intracranial haemorrhage, with bleeding in or around the brain (haemorrhagic stroke)
154
Q

The blood supply to the brain may be disrupted by:

A
  • A thrombus or embolus
  • Atherosclerosis
  • Shock
  • Vasculitis
155
Q
A
156
Q

What is a Transient ischaemic attack (TIA)

A

Transient ischaemic attack (TIA) involves temporary neurological dysfunction (lasting less than 24 hours) caused by ischaemia but without infarction.

157
Q

Symptoms for TIA

A

Symptoms have a rapid onset and often resolve before the patient is seen. TIAs may precede a stroke

158
Q

What is Crescendo TIAs

A

Crescendo TIAs are two or more TIAs within a week and indicate a high risk of stroke.

159
Q

Presentation stroke

A

A sudden onset of neurological symptoms suggests a vascular cause (e.g., stroke). Stroke symptoms are typically asymmetrical. Common symptoms are:

  • Limb weakness
  • Facial weakness
  • Dysphasia (speech disturbance)
  • Visual field defects
  • Sensory loss
  • Ataxia and vertigo (posterior circulation infarction)
160
Q

RF for stroke

A
  • Previous stroke or TIA
  • Atrial fibrillation
  • Carotid artery stenosis
  • Hypertension
  • Diabetes
  • Raised cholesterol
  • Family history
  • Smoking
  • Obesity
  • Vasculitis
  • Thrombophilia
  • Combined contraceptive pill
161
Q

What is the FAST tool

A

The FAST tool is used as a simple way to identify stroke in the community:

F – Face
A – Arm
S – Speech
T – Time (act fast and call 999)

162
Q

What is a ROSIER Tool

A

The ROSIER tool (Recognition Of Stroke In the Emergency Room) gives a score based on the clinical features and duration. Stroke is possible in patients scoring one or more.

163
Q

Management of TIA

A

Symptoms should have completely resolved within 24 hours of onset. Initial management involves:

  • Aspirin 300mg daily (started immediately)
  • Referral for specialist assessment within 24 hours (within 7 days if more than 7 days since the episode)
  • Diffusion-weighted MRI scan is the imaging investigation of choice
164
Q

Management of Stroke

A

The information here is summarised from the NICE guidelines (updated 2022) on stroke. Initial management involves:

  • Exclude hypoglycaemia
  • Immediate CT brain to exclude haemorrhage
  • Aspirin 300mg daily for two weeks (started after haemorrhage is excluded with a CT)
  • Admission to a specialist stroke centre
165
Q

When can you use thrombolysis in stroke?

A

Thrombolysis with alteplase is considered once haemorrhage is excluded (after the CT scan). Alteplase is a **tissue plasminogen activator **that rapidly breaks down clots. It may be given within 4.5 hours of the symptom onset, based on local protocols and by an appropriately trained team. Patients need close monitoring for complications, particularly intracranial or systemic haemorrhage, with access to immediate imaging if bleeding is suspected.

166
Q

When is thrombectomy used in stroke?

A

Thrombectomy is considered in patients with a confirmed blockage of the proximal anterior circulation or proximal posterior circulation. It may be considered within 24 hours of the symptom onset and alongside IV thrombolysis.

167
Q

TRUE OR FALSE

In patients with an ischaemic stroke, lowering the blood pressure can better the ischaemia.

A

FALSE
In patients with an ischaemic stroke, lowering the blood pressure can worsen the ischaemia.
High blood pressure treatment is only indicated in hypertensive emergency or to reduce the risks when giving intravenous thrombolysis. Blood pressure is aggressively treated in patients with a haemorrhagic stroke

168
Q

Patients with a TIA or stroke are investigated for carotid artery stenosis and atrial fibrillation with:

A
  • Carotid imaging (e.g., carotid ultrasound, or CT or MRI angiogram)
  • ECG or ambulatory ECG monitoring
169
Q

Surgical interventions are considered where there is significant carotid artery stenosis. The options are:

A
  • Carotid endarterectomy (recommended in the NICE guidelines)
  • Angioplasty and stenting
170
Q

The top risk factors to remember for stroke are

A

atrial fibrillation and carotid artery stenosis.

171
Q

Secondary Prevention for Stroke/TIA

A
  • Clopidogrel 75mg once daily (alternatively aspirin plus dipyridamole)
  • Atorvastatin 20-80mg (not started immediately – usually delayed at least 48 hours)
  • Blood pressure and diabetes control
  • Addressing modifiable risk factors (e.g., smoking, obesity and exercise)
172
Q

Stroke patients require a period of adjustment and rehabilitation involving a multi-disciplinary team of:

A
  • Stroke physicians
  • Nurses
  • Speech and language (SALT) to assess swallowing
  • Dieticians in those at risk of malnutrition
  • Physiotherapy
  • Occupational therapy
  • Social services
  • Optometry and ophthalmology
  • Psychology
  • Orthotics