Neurology Flashcards

1
Q

How can you reposition the bed to reduced ICP in patients with head injuries?

A

Reposition the bed to 30 degrees.

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2
Q

Cushing’s triad.

A

Bradycardia
Hypertension
Irregular respirations (abnormal breathing patterns—>Cheyne-Stokes)

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3
Q

Spinal cord compression immediate management.

A

Immobilise and administer corticosteroids (e.g., dexamethasone) to reduce inflammation/oedema.

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4
Q

Lewy-Body dementia may cooccur with which neurodegenerative condition?

A

Parkinson’s disease.

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5
Q

Parkinson’s pathophysiology.

A

Depletion of dopaminergic neurones in the substantia nigra pars compacta.

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6
Q

A mutation of what gene causes Rett Syndrome?

A

MECP2

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7
Q

Central necrosis is a common feature of what type of brain tumour?

A

Glioblastoma multiforme.

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8
Q

Bell’s palsy gold-standard treatment.

A

Steroids (prednisolone) within 72 hours of onset of symptoms.

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9
Q

Bell’s palsy gold-standard treatment.

A

Steroids (prednisolone) within 72 hours of onset of symptoms.

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10
Q

Is the onset of Bell’s palsy rapid or slow?

A

Rapid

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11
Q

A 55-year-old man presents with a 2-month history of progressive headaches, nausea, and speech difficulties. His family notes occasional confusion. Neurological exam shows mild right-sided weakness and papilloedema.

A CT scan reveals a large, irregular, heterogeneously enhancing mass with central necrosis and surrounding vasogenic oedema in the left frontal lobe.

What are the next steps in the management of this patient?

A
  1. Multidisciplinary Team (MDT) Assessment: Refer the patient to a specialist MDT for comprehensive evaluation and management planning.
  2. Surgical Resection: If feasible, perform surgical resection to reduce tumor burden and alleviate symptoms.
  3. Radiotherapy: Administer radiotherapy, typically 60 Gy in 30 fractions, with concomitant temozolomide. For patients aged around 70 or over, or those with a Karnofsky performance status of less than 70, consider 40 Gy in 15 fractions.
  4. Adjuvant Temozolomide: Offer up to 6 cycles of adjuvant temozolomide for patients with MGMT methylation-positive tumors. For those with MGMT methylation-negative tumors or unknown status, consider up to 12 cycles of adjuvant temozolomide.
  5. Supportive Care: Provide supportive care to manage symptoms and improve quality of life.
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12
Q

Sensory loss on the dorsal aspect of the 1st and 2nd metacarpals suggest damage to what nerve?

A

Radial nerve

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13
Q

What are the common causes of spinal cord compression?

A

> Degenerative Diseases: Such as osteoarthritis.

> Injuries: Trauma to the spine.

> Tumours: Both benign and malignant growths.

> Infections: Infections in the spine causing swelling.

> Other Conditions: Scoliosis, rheumatoid arthritis, and certain bone diseases.

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14
Q

Describe the typical pain characteristics associated with spinal cord compression.

A

Severe and Localised Pain: Often in the neck, back, or lower back.

Aggravated by Movement: Pain worsens with activities like coughing, sneezing, or straining.

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15
Q

What are the key neurological signs that indicate spinal cord compression?

A

> Motor Deficits: Weakness or paralysis in the limbs below the level of compression.

> Sensory Loss: Numbness or loss of sensation, often in a dermatomal pattern.

> Upper Motor Neuron Signs: Hyperreflexia, spasticity, clonus, and a positive Babinski sign.

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16
Q

How does spinal cord compression differ from cauda equina syndrome in terms of symptoms and signs?

A

Spinal Cord Compression:
Location: Typically higher up in the spinal cord.

Symptoms: Upper motor neurone signs such as hyperreflexia, spasticity, and a positive Babinski sign.

Cauda Equina Syndrome:
Location: Involves the nerve roots at the lower end of the spinal cord (lumbar and sacral regions).

Symptoms: Lower motor neurone signs such as hyporeflexia, flaccid paralysis, saddle anaesthesia, and bowel/bladder dysfunction.

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17
Q

How does therapeutic hyperventilation work to lower ICP?

A

1) Hyperventilation: this process involves increasing the patient’s breathing rate, which lowers PaCO2 levels in the blood.

2) Cerebra Vasoconstriction: the reduction in PaCO2 causes cerebral vasoconstriction.

3) Decreased Cerebral Blood Flow (CBF): vasoconstriction reduces the amount of blood flowing to the brain.

4) Reduced Cerebral Blood Volume: with less blood in the brain, the overall volume inside the skull decreases.

5) Lower ICP: the decrease in cerebral blood volume leads to a reduction in ICP.

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18
Q

Lambert-Eaton Myasthenic Syndrome (LEMS).

A

> Can be paraneoplastic or autoimmune.
Unlike MG, antibodies are to presynaptic voltage-gated calcium channels.

Clinical features:
>Gait difficulty before eye signs.
>Autonomic involvement (xerostomia, constipation, impotence).
>Hyporeflexia and weakness, which improve after exercise.
>Diplopia and respiratory muscle involvement are rare.
>EMG shows similar changes to MG except amplitude increases greatly post-exercise.

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19
Q

LEMS management.

A

Pyridostigmine, 3,4-diaminopyridine or IVIg (get specialist help).

Do regular CXR/high-resolution CT as symptoms may precede cancer by >4 years.

20
Q

Risk factors for migraines.

A

> High frequency episodic migraine.
Overuse of acute migraine medications.
Excessive caffeine consumption.
Obesity.
Snoring and sleep disorders.
Comorbid condition, such as head injury, pain disorders, anxiety, and depression.
Major life events, such as marriage or job loss.
Chocolate.
Oral contraceptives.
Alcohol.
Exercise.
Menstruation.

21
Q

What is a migraine?

A

A migraine is a common, chronic neurological disorder characterised by recurrent episodes of moderate to severe headaches, often accompanied by nausea, vomiting, and sensitivity to light or sound.

22
Q

How does cortical spreading depression relate to migraines?

A

A wave of neuronal and glial depolarisation spreads across the cortex, leading to aura symptoms and changes in blood flow.

23
Q

What age group is most commonly affected by migraines?

A

Migraines are most common between the ages of 25-55.

24
Q

How does gender influence the prevalence of migraines?

A

Females are 2-3 times more likely than men to have migraines.

25
Q

How are migraines diagnosed?

A

Migraines are primarily diagnosed based on clinical history and physical examination, as there is no definitive test.

26
Q

How might older people present with migraines differently?

A

Older people may present with aura without the proceeding headache, and further investigation may be indicated to rule out serious conditions like TIA.

27
Q

What are some typical aura symptoms?

A

Transient hemianopic disturbance
Spreading scintillating scotoma

28
Q

What are prodromal symptoms of migraines?

A

Symptoms occurring hours to days before the headache, such as fatigue, mood changes, neck stiffness, and yawning.

29
Q

Describe the clinical features of a migraine.

A

Severe unilateral (or bilateral), throbbing headache
Attacks may last up to 72 hours
Associated with nausea, photophobia, and phonophobia
Patients typically seek a dark, quiet room during an attack
Pain aggravated by physical activity

30
Q

What is an aura in the context of migraines?

A

An aura is a set of symptoms that can occur with or without headache, are fully reversible, develop over at least 5 minutes, and typically last 5-60 minutes. They are often visual and progressive.

31
Q

What are postdromal symptoms of migraines?

A

Symptoms such as fatigue or elated/depressed mood that can last for up to 48 hours after the headache.

32
Q

First-line acute treatment of migraine.

A

Combination therapy:

> Oral triptan + NSAID.
Oral triptan + paracetamol.

In people aged 12-17, consider nasal triptan instead.

If patient prefers monotherapy, consider oral triptan, NSAID, paracetamol, aspirin 900mg alone.

Opioids should NOT be offered to patients with migraine.

33
Q

When should patients with migraine with aura take triptan?

A

They should take the triptan at the start of the headache, not at the onset of aura (unless these occur together).

34
Q

What is the second-line acute treatment of migraines?

A

If the first line is ineffective, add non-oral metoclopramide or prochlorperazine.

35
Q

Preventative treatment of migraines.

A

Options include:
Propanolol OR topiramate.
Amitriptyline.

Avoid topiramate in women of childbearing age.

If this is still not effective as prophylaxis, offer sessions of acupuncture or riboflavin.

36
Q

Monitoring for migraines after starting treatment.

A

The patient should be followed up within 2-8 weeks of commencing treatment.

37
Q

Prognosis of migraines.

A

Migraines are a chronic condition with variable prognosis.

> Frequency and severity of attacks may decrease with age.

> Some individuals may experience chronic migraine, defined as headaches on 15 or more days per month.

> In pregnancy, 80% of women with migraine report an improvement in symptoms once 2nd and 3rd trimester starts.

38
Q

Complications of migraines.

A

> Medication-overuse headache: regular use of acute migraine medications can lead to worsening headache frequency and chronic daily headaches.

> Migraine is the underlying cause in about 80% of cases.

> Reduced functional ability and quality of life, impacting social life, education, and employment.

> Chronic migraine: progression from episodic to chronic migraine is associated with significant disability and comorbidities.

> Increased risk of stroke (ischaemic and haemorrhagic).

> Ischaemic strike is doubled in migraine sufferers.

> Haemorrhagic stroke risk is 50% higher in migraine patients.

> Risk further increases with combined hormonal contraception in women.

> Status migrainosus: debilitation migraine lasting over 72 hours.

> Migrainous infarction: aura symptoms over 60 minutes with ischaemic brain lesion evidence.

> Migraine aura-triggered seizure.

> Pregnancy complications: increased risk of pre-eclampsia, central venous sinus thrombosis, preterm birth, and low birth weight.

> Depression.

39
Q

What is status migrainosus?

A

A migraine attack that lasts longer than 72 hours.

40
Q

Medication-overuse headache (MOH).

A

Also known as a rebound headache, an MOH occurs when pain relief medications are used too frequently to treat headaches, such as migraines.

Causes:
Typically happens when painkillers are taken more than a couple of days a week. This frequent use can lead to a cycle where the headache improves with medication but returns as the medication wears off.

Symptoms:
These headaches often occur daily and can be very painful. They may wake you up early in the morning and are often accompanied by symptoms like nausea, restlessness, trouble concentrating, memory problems, and irritability.

Risk Factors:
People with a history of headache disorders, such as migraines or tension-type headaches, are more prone to developing MOH.

Treatment:
The most effective way to treat MOH is to stop taking the overused medication. This can be challenging initially, but healthcare providers can offer support and alternative treatments to manage the headaches.

41
Q

List some CGRP monoclonal antibodies.

A

> Erenumab
Galcanezumab
Fremanezumab

42
Q

A 72-year-old woman presents to the clinic with a 3-week history of severe, throbbing headaches localized to her right temple. She describes the pain as constant and worsening, often waking her up at night. She also reports jaw claudication, particularly when chewing, and has noticed some visual disturbances, including transient episodes of blurred vision in her right eye. She has experienced fatigue, low-grade fever, and unintentional weight loss of 5 kg over the past month.

Physical Examination:

Vital signs: BP 140/85 mmHg, HR 88 bpm, Temp 37.8°C.
General: Appears tired and in mild distress.
HEENT: Tenderness over the right temporal artery, which is thickened and has reduced pulsation.
Neurological: No focal deficits.
Laboratory Findings:

ESR: 85 mm/hr (elevated)
CRP: 45 mg/L (elevated)
Hemoglobin: 11.2 g/dL (mild anemia)

Given the patient’s presentation, what is the most likely diagnosis, and what is the next best step in management?

A. Temporal artery biopsy B. MRI of the brain C. High-dose corticosteroids D. Lumbar puncture E. Nonsteroidal anti-inflammatory drugs (NSAIDs)

A

C. High-dose corticosteroids.
The best next step is to start high-dose corticosteroids immediately to prevent complications such as permanent vision loss. Temporal artery biopsy should be performed to confirm the diagnosis, but treatment should not be delayed while awaiting biopsy.

43
Q

What are the complications of GCA?

A

Vision loss: one of the most feared complications is sudden, painless vision loss in one or both eyes due to reduced blood flow to the optic nerve. This vision loss is often permanent.

Aortic aneurysm: GCA can cause inflammation of the aorta, leading to the formation of an aneurysm. This is a bulge in the weakened wall of the aorta, which can potentially rupture and cause life-threatening bleeding.

Stroke: although less common, GCA can lead to a stroke due to inflammation and narrowing of the arteries that supply blood to the brain.

Other vascular complications: these include stenosis of other large arteries, which can lead to symptoms like limb claudication (pain due to inadequate blood flow), mesenteric ischaemia, and even arterial thrombosis.

Polymyalgia rheumatica: about 50% of people with GCA also have PMR, which causes pain and stiffness in the neck, shoulders, and hips.

44
Q

What are the symptoms of GCA?

A

> Headache: Persistent, severe head pain, usually in the temple area.
Scalp Tenderness: Pain or sensitivity when touching the scalp.
Jaw Claudication: Pain in the jaw when chewing or talking.
Vision Problems: Blurred vision, double vision, or sudden, permanent vision loss in one eye.
Fever: Low-grade fever is common.
Fatigue: General feeling of tiredness and lack of energy.
Unintended Weight Loss: Losing weight without trying.
Polymyalgia Rheumatica (PMR): Pain and stiffness in the neck, shoulders, and hips.

45
Q

First-line imaging test for GCA and what sign would be seen?

A

Temporal artery ultrasound. A ‘halo sign’ indicates inflammation.

MRI or CT angiography used to assess large vessel involvement if suspected.

46
Q

Definitive diagnosis of GCA.

A

Temporal artery biopsy. This is considered the gold standard for diagnosing GCA. It should be performed promptly but treatment with corticosteroids should not be delayed while awaiting biopsy results.

47
Q

Immediate treatment of GCA. Provide prescribing information.

A

High-dose corticosteroids.

Prednisolone PO
40-60mg daily until remission of disease activity, the higher dose being used if visual symptoms occur; maintenance 7.5-10mg daily, reduce gradually to maintenance dose.

Many patients require treatment for at least 2 years and in some patients it may be necessary to continue long-term low-dose steroids.