Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Phase 2A > Neurology > Flashcards

Neurology Flashcards

1
Q

What constitutes the CNS?

A

The brain and spinal cord

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What constitutes the PNS?

A

The cranial nerves and the other nerves in the body not in the spinal cord.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What are the physiological divisions of nerves?

A

Somatic (sensory and motor)
Branchial (motor only)
Autonomic (sensory and motor)
Special senses (sensory only) - olfaction, vision, accelerometer etc.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What are the three different functional types of motor neurones?

A

Somatic, autonomic and branchial

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What are the three different functional types of sensory neurones?

A

Somatic, autonomic and special

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What is a dermatome?

A

An area of skin supplied by a single spinal nerve/pair of nerves

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What is a myotome?

A

A volume of muscle supplied by a single spinal nerve

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What is the spinal cord?

A

The pathway for motor control from the brain to the body and the pathway for sensory information from the body to the brain.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What percentage of strokes are embolic?

A

85%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What percentage of strokes are haemorrhagic?

A

10%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What are the rarer causes of strokes?

A

Vasculitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What is the typical presentation of an intracerebral haemorrhage?

A

Sudden onset headache, drowsiness, vomiting, focal deficit

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What are the primary causes of ICH?

A

Hypertension - Charcot-Bouchard aneurysms

Amyloid angiopathy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What are the secondary causes of ICH?

A

Tumour, AVM, cerebral aneurysm, haemorrhagic transformation infarct, venous infarct, anticoagulants

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What locations of ICH are typical of hypertensive bleeds?

A

Basal ganglia
Pons
Cerebellum

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What are the three complications of Charcot-Bouchard aneurysms?

A

Rupture, thrombosis and leakage

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What complication does intraventricular extension cause?

A

Hydrocephalus as the brain cannot resorb CSF

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What is the management of an anticoagulant-related ICH?

A

Discuss with haematologist
If on warfarin check INR and consider reversal with Beriplex and Vit K
If has low platelets - consider transfusion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What imaging can be used post-stroke?

A

CTA, MRA, catheter angiography

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Why is imaging used post-stroke?

A

To look for causes of the ICH e.g. vascular abnormalities, tumours or microbleeds

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What are the symptoms of an ACA stroke?

A 
Leg weakness
Sensory disturbance in the legs
Gait apraxia - truncal ataxia
Incontinence
Drowsiness
Akinetic Mutism
- decrease in spontaneous speech
- stuporous state
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What are the symptoms of an MCA stroke?

A 
Contralateral arm and leg weakness
Contralateral sensory loss
Hemianopia
Aphasia
Dysphasia
Facial droop
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What are the symptoms of a PCA stroke?

A

Contralateral homonymous hemianopia
Cortical blindness with bilateral involvement of the occipital lobe branches
Visual agnosia
Prosopagnosia - face blindness
Dyslexia, anomic aphasia, colour naming and discrimination problems
Headaches unilateral

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What are the symptoms of a posterior circulation stroke?

A 
Motor deficits such as hemiparesis or tetraparesis and facial paresis
Dysarthria and speech impairment
Vertigo, nausea and vomiting
Visual disturbances
Altered consciousness
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What is the treatment for an ischaemic stroke?

A

Thrombolysis (up to 4.5 hours post onset of symptoms)
Clot retrieval
Intra-arterial thrombolysis
Decompressive craniectomy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What are the contraindications of thrombolysis?

A 
Recent surgery in the last 3 months
Recent arterial puncture
History of active malignancy
Evidence of brain aneurysms
Patient on anticoagulation
Severe liver disease
Acute pancreatitis 
Clotting disorder
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Name 3 types of primary headache.

A

Migraine
Cluster
Tension type

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Name 3 types of secondary headaches.

A 
Meningitis
Subarachnoid haemorrhage
Giant cell arteritis
Idiopathic intracranial hypertension
Medication overuse headache - caused by overuse of OTC medications
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Under what circumstances would you consider immediate referral to a neurologist regarding a headache?

A 
Thunderclap headache - ?SAH
Seizure and new headache
?meningitis
?encephalitis 
Red eye - ?acute glaucoma
Headache and new focal neurology including papilloedema
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

What are the red flags with headache?

A 
New headache with a history of cancer
Cluster headache
Seizure
Significantly altered consciousness, memory, confusion, coordination
Papilloedema 
Other abnormal neuro exam of symptoms
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

What are the different types of common headache?

A

Migraine (episodic with and without aura; chronic migraine)
Medication overuse
Tension type headache

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

What is the abortive treatment for migraine?

A

An oral triptan and an NSAID or an oral triptan and paracetamol
Consider an anti-emetic, even in the absence of N&V.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

What is the preventative treatment of migraine?

A

Topiramate or propanolol, amitriptyline. Advise patients to take 400 mg riboflavin OD.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

What do nerve conduction studies assess?

A

The peripheral nervous system

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

What can nerve conduction studies show?

A

Axon loss - small responses

Myelin loss - slow responses

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

What is electromyography used for?

A

To determine whether a PNS problem is in the nervous system or muscle. The NCS is normal even though the patient is weak, the problem is with the muscle.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

What are EEGs used for?

A

Primarily done for patients with seizures.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

What do somatosensory evoked potentials examine?

A

Look at the integrity of the dorsal columns.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

How do somatosensory evoked potentials work?

A

You stimulate the peripheral nerve and record a response from the somatosensory cortex using scalp electrodes, like an EEG.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

What do visual evoked potentials examine?

A

The visual pathways

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

What are visual evoked potentials used for?

A

To look for demyelination in the optic nerve in conditions such as MS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

What are somatosensory evoked potentials used for?

A

To diagnose MS and intraoperative monitoring e.g. in spinal cord surgery

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

What is transcranial magnetic stimulation?

A

A brief magnetic pulse induces an electric current that excites cells in the motor cortex.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

What are the main uses of transcranial magnetic stimulation?

A

To diagnose motor neuron disease, MS and to treat severe depression.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

What is meningitis?

A

Inflammation of the meninges; it can be bacterial, viral or fungal.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

What is encephalitis?

A

Inflammation of the brain, it is usually viral

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

What is encephalopathy?

A

A reduced level of consciousness/diffuse disease of brain substance, usually non-infective but has multiple aetiologies.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

What is neuropathy?

A

Damage to the peripheral nerve e.g. diphtheria, Guillain-Barre syndrome, Lyme disease and Hep A

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

What is polyradiculopathy?

A

Inflammation of the nerve roots e.g. in cauda equina, HIV + CMV/syphilis/HSV

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

What is myelitis?

A

Inflammation of the spinal cord (whole cord cross section vs. anterior horn cells)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

What is meningoencephalitis?

A

It resembles both meningitis and encephalitis.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

What are the clinical signs of meningeal irritation?

A

Reduced GCS
Headache
Neck stiffness
Papilloedema
Kernie’s sign (extension of the knee is painful when the hip is flexed)
Burdzinski’s sign (severe neck stiffness causes a patient’s hips and knees to flex when the neck is flexed

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

What are the important steps in the management of meningeal irritation?

A 
Blood cultures before antibiotics
Antibiotics
Bloods: FBC, U&E, CRP, serum glucose, lactate
Lumbar puncture
CT head
Throat swabs (bacterial and viral)
Pneumococcal and meningococcal serum PCR
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

What are the important adverse effects of a lumbar puncture?

A 
Headache
Parasthesia
CSF leak
Damage to the spinal cord
Cerebral herniation and death
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

What investigations should be performed on CSF for ?meningitis?

A 
CSF protein and glucose
MC&S
Viral PCR (enterovirus, HSV/VZV)
Bacterial PCR
Simultaneous serum glucose
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

What are the common bacterial causes of meningitis in children and adults?

A

Neisseria meningitides
Streptococcus pneumoniae
Listeria monocytogenes
Haemophilus influenzae

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

What are the common bacterial causes of meningitis in neonates?

A

E. coli (gut flora can spread easily in a neonate)
Group B streptococci (carried by some women in the vagina)
Listeria monocytogenes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

What is the management for suspected bacterial meningitis?

A

IV Cefotaxime (or ceftriaxone; chloramphenicol if the patient has severe anaphylaxis with beta-lactams)
Add amoxicillin IV for listeria cover if >55, immunocompromised or the patient has a Hx of alcohol excess
Add steroids
Consider vancomycin in return travellers

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

What forms of meningitis don’t require prophylaxis

A

Those caused by H. influenzae and pneumococcal bacteria if the patient has been vaccinated.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

What is meningococcal sepsis?

A

Meningitis and septicaemia where the bacteria are in the blood; this is a medical emergency.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

What is the treatment for viral meningitis?

A

There is no specific treatment, treatment is just supportive.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

What is the management of encephalitis?

A

Treat empirically with IV acyclovir.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

What are the symptoms of encephalitis?

A

Fever
Headache
Lethargy
Behavioural change

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

What are the symptoms of rabies?

A 
Fever
Anxiety
Confusion
Hydrophobia
Hyperactivity/uncontrollable excitement
Hallucinations
Violent movements
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

What are the symptoms of tetanus?

A 
Paraesthesia of the wound
Lockjaw
Sustained muscle contractions
Involvement of the facial muscles
Paroxysmal generalised spasms
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

What are the symptoms of Clostridium botulinum infection?

A 
Descending paralysis with cranial neuropathy first then:
Diplopia
Dysarthria
Dysphagia
Peripheral weakness
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

What is the aetiology of a TIA?

A

It is usually embolic but it may be thrombotic. The most common source of emboli is the carotids, usually the bifurcation. It can also originate with AF and valve disease.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

What is the pathophysiology involved in a TIA?

A

There is temporary inadequacy of the circulation in part of the brain leading to a cerebral or retinal deficit. It doesn’t last >24 hours and most last <30 minutes.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

What are the risk factors associated with TIA?

A

HTN, smoking, DM, heart disease, peripheral arterial disease, polycythaemia vera, combined OCP, hyperlipidaemia, excess alcohol, clotting disorders

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

Which gender experiences more TIAs?

A

Males

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

What are the symptoms of a TIA?

A

Unilateral weakness, unilateral sensory loss, drooping face, confusion, difficulty with speech, amaurosis fugax (painless, fleeting loss of vision)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
72
Q

What are the signs of a TIA?

A

Dysarthria (difficulty with speech), dysphagia, loss of memory, abnormal behaviour, homonymous hemianopia, diplopia, ataxia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
73
Q

What tests are used to diagnose a TIA?

A

A TIA is a retrospective diagnosis as it is only once it’s over that it’s diagnosed as a TIA
Bloods: FBC, ESR, U&Es, fasting lipids and glucose, LFTs, TSH
ECG - may show AF, MI or evidence of myocardial ischaemia
Imaging - carotid doppler
ABCD2 score - predicts risk of a stroke

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
74
Q

What is the treatment for a stroke?

A

Control cardiovascular risk factors e.g. HTN, hypercholesterolaemia, smoking cessation
Clopidogrel
Carotid endarterectomy if stenosis is >70%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
75
Q

What is the aetiology of a stroke?

A

Young patient: vasculitis, thrombophilia, SAH, venous sinus thrombosis, carotid artery dissection
Older patient: thrombosis, thromboembolism, CNS bleed, vasculitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
76
Q

What is the pathophysiology of a stroke?

A

A stroke is due to disruption of the blood supply caused by ischaemic infarction of part of the brain or from intracranial haemorrhage

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
77
Q

What are the risk factors for a stroke?

A

HTN, smoking, DM, heart disease, peripheral arterial disease, polycythaemia vera, combined OCP, hyperlipidaemia, excess alcohol, clotting disorders, post-TIA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
78
Q

What is the epidemiology of a stroke?

A

Most occur in patients >65

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
79
Q

What are the symptoms of a stroke?

A

Facial drooping, weakness in a limb or side of the body, hemisensory loss, dysphagia, diplopia, ataxia, imbalance, unsteadiness, dysarthria

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
80
Q

What are the signs of a stroke?

A

Nystagmus, Horner’s syndrome, hemianopia, flaccid paralysis (becomes spastic later), locked in syndrome - complete infarction affecting the pons

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
81
Q

What tests are used to diagnose a stroke?

A

Bloods: FBC, ESR, glucose and lipids
Imaging - head CT, MRI head, carotid doppler, cerebral angiography
Echo if suspected cardiac emboli
ECF - AF

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
82
Q

What is the treatment for a stroke?

A

Ischaemic - thrombolysis (IV alteplase, must be given <4.5 hours from onset), aspirin for 2 weeks then clopidogrel
Haemorrhagic - BP control, beta blockers, Beriplex if it’s warfarin related, clot evacuation
Risk factor management e.g. antihypertensives, statins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
83
Q

What are the risk factors for a SAH?

A

HTN, smoking, cocaine use, excess alcohol, Ehlers-Danlos syndrome (type 4), ADPKD and neurofibromatosis (type 1) - all genetic conditions associated with aneurysms

84
Q

What is the pathophysiology involved in a SAH?

A

It is usually a result of bleeding from a Berry aneurysm, there is spontaneous arterial bleeding into the subarachnoid space

85
Q

What is the epidemiology of SAH?

A

Women > men

86
Q

What are the symptoms of a SAH?

A

Sudden onset severe headache, loss of consciousness, photophobia, seizures, nausea and vomiting, diplopia

87
Q

What are the signs of a SAH?

A

Positive signs of meningism e.g. Kernig’s sign (painful knee extension when the thigh is flexed), neck stiffness, papilloedema.

88
Q

What tests are used to diagnose a SAH?

A

Head CT without contrast - white star shape
Angiography
LP - xanthochromia (yellow discolouration of the CSF)
ECG

89
Q

What is the treatment for a SAH?

A

Refer to neurosurgery - clip or coil the aneurysm
Supportive treatment e.g. intubation and ventilation if necessary (+/- NG feeding)
Analgesia and antiemetics for conscious patients

90
Q

What are the complications of a SAH?

A

Cerebral ischaemia and hydrocephalus

91
Q

What is the aetiology of a subdural haemorrhage?

A

Blunt head trauma e.g. banging the head on the floor after falling is the usual mechanism of injury; can be acute, subacute (3-7 days post injury) or chronic (2-3 weeks post injury)

92
Q

What is the pathophysiology involved in a subdural haemorrhage?

A

There is tearing of the bridging veins from the cortex to one of the draining venous sinuses. Days/weeks later the haematoma starts to autolyse causing an increase in oncotic pressure and osmotic pressure, water enters the heamatoma and causes a gradual increase in ICP

93
Q

What is the epidemiology involved in a subdural haemorrhage?

A

Incidence increases with age

94
Q

What are the symptoms of a subdural haemorrhage?

A

Headache, seizures, vomiting, nausea, anorexia, increasing drowsiness/confusion, speech difficulties

95
Q

What are the signs of a subdural haemorrhage?

A

Papilloedema, bradycardia, hypertension, bruising or purpura

96
Q

What tests are used to diagnose a subdural haemorrhage?

A

Bloods: FBC, U&Es, LFTs, clotting screen - could show coagulopathy
CT head - crescent shaped mass and midline shift

97
Q

What is the treatment for a subdural haemorrhage?

A

Refer to neurosurgery - clot evacuation and craniotomy
Hypertonic saline or mannitol can be used to treat increased ICP
Treat any coagulopathy

98
Q

What is the aetiology of an extradural haemorrhage?

A

It is most often due to a fractured temporal or parietal bone damaging the middle meningeal artery or vein; they can also occur in the spinal column

99
Q

What is the pathophysiology involved in an extradural haemorrhage?

A

There is a collection of blood between the dura and bone, usually the skull but can be the spine

100
Q

What is the epidemiology of an extradural haemorrhage?

A

Males > females

101
Q

What are the symptoms of an extradural haemorrhage?

A

Loss of consciousness, severe headache, vomiting, seizures, confusion, nausea, coma
Weakness, numbness, urinary and/or faecal incontinence - spinal EDH

102
Q

What are the signs of an extradural haemorrhage?

A

Bradycardia +/- hypertension, CSF otorrhoea or rhinorrhoea, unequal pupils.
Patients are often knocked unconscious at the time of injury, have a lucid interval and then deteriorate

103
Q

What tests are used to diagnose an extradural haemorrhage?

A

XR of the skull - might show a fracture
CT head - lentiform shaped mass
Bloods
Avoid an LP

104
Q

What is the treatment for an extradural haemorrhage?

A

ABCDE
Protect the neck until injury has been excluded
Refer to neurosurgery - evacuate the haematoma
Raised ICP can be treated with hypertonic saline and mannitol

105
Q

What is the cause of epilepsy?

A

Most cases are idiopathic but epilepsy can also be caused by CVA, head injury, CNS infections, autoimmune disease, brain neoplasm, genetic diseases and drugs

106
Q

What is the pathophysiology involved in epilepsy?

A

There is a sudden, synchronous discharge of cerebral neurons causing symptoms/signs of abnormal electrical activity.

107
Q

What are the symptoms of epilepsy?

A

Seizure-related symptoms include sudden falls, involuntary jerky movements of limbs whilst awake, blank spells, unexplained incontinence of urine, deja vu, fear, premonition, olfactory, gustatory, visual or auditory hallucinations, post-ictal symptoms

108
Q

What are the signs of epilepsy?

A

There are no obvious physical signs

109
Q

What tests are used to diagnose epilepsy?

A

Bloods: FBC, U&Es, glucose, serum calcium, LFTs, renal function
EEG, sleep recordings or 24 hour ambulatory EEG, inpatient EEG videotelemetry
MRI of the head

110
Q

What is the treatment for epilepsy?

A

Focal - carbamazepine (inhibits Na channels) or lamotrigine (inhibits glutamate release)
Generalised - sodium valproate (inhibits Na channels) or lamotrigine

111
Q

What is status epilepticus?

A

It is a medical emergency which occurs when someone has had a seizure longer than 30 minutes or 2 or more seizures without recovery of consciousness between them over a similar period. There is risk of permanent cerebral damage.

112
Q

What is the aetiology of Parkinson’s disease?

A

It is mostly idiopathic, there is a small increased risk with rural living and drinking well water; pesticide exposure increases risk

113
Q

What is the pathophysiology involved in Parkinson’s disease?

A

Pathological hallmarks are the presence of neuronal inclusions - Lewy bodies and loss of the dopaminergic neurones in the substantia nigra

114
Q

What are the symptoms of Parkinson’s disease?

A

Tremor at rest, rigidity, bradykinesia, impairment of dexterity, fixed facial expression and infrequent blinking, cognitive impairment - PD dementia

115
Q

What are the signs of Parkinson’s disease?

A

Progressive fatiguing and reduction in amplitude of repetitive movements, pill-rolling tremor, stooped posture, reduced arm swing on 1 side, shufflinf

116
Q

What tests are used to diagnose Parkinson’s disease?

A

Parkinson’s disease is a clinical diagnosis and is made by a neurologist upon a thorough neurological examination. MRI is normal but not necessary in typical cases.

117
Q

What is the treatment for Parkinson’s disease?

A

Medication - Levodopa, dopamine agonists e.g. rotigotine, monoamine oxidase inhibitors e.g. selegiline
Deep brain stimulation

118
Q

What is the aetiology of Huntington’s chorea?

A

Huntington’s disease is an autosomal dominant disease due to CAG trinucleotide repeat expansion in huntingtin, the protein gene product.

119
Q

What is the pathophysiology involved in Huntington’s chorea?

A

There is cell loss within the basal ganglia and cortex, loss of GABAergic and cholinergic neurones

120
Q

What are the symptoms of Huntington’s chorea?

A

Personality change, self-neglect, apathy and clumsiness, depression, fidgeting with fleeting facial grimaces and then chorea (abnormal, involuntary movements) and dementia

121
Q

What are the signs of Huntington’s chorea?

A

Progressive chorea, rigidity and dementia, seizures, dystonia, Parkinsonian features, cardiomyopathy, skeletal muscle wasting, pyramidal tract signs

122
Q

What tests are used to diagnose Huntington’s chorea?

A 
Imaging - MRI or CT in moderate-severe disease shows a loss of striatal volume and increased size in the frontal horns of the lateral ventricles
Genetic testing (and extensive genetic counselling)
123
Q

What is the treatment for Huntington’s chorea?

A

There is NO cure or disease-modifying treatments, just symptom control
Chorea: sulpiride - atypical antipsychotic
Depression: SSRIs e.g. citalopram, paroxetine
Aggression: Risperidone - antipsychotic

124
Q

What are some triggers for migraine?

A 
CHOCOLATE
Chocolate, cheese
Hangovers
OCP
Caffeine
Orgasms 
Lie ins
Alcohol 
Travel
Exercise
125
Q

What is the pathophysiology involved in migraines?

A

They are thought to be primarily neurogenic rather than vascular.

126
Q

What are the three main types of migraine?

A

Migraine with aura
Migraine without aura
Migraine aura without headache

127
Q

What are the symptoms of a migraine?

A

Unilateral headache, pulsing pain, moderate-severe headache, aggravation by routine physical activity

128
Q

What are the signs of a migraine?

A

Aura - visual, auditory or motor (rare), nausea and/or vomiting, photophobia.
Lasts 4-72 hours

129
Q

What tests are used to diagnose a migraine?

A

A full history and examination is all that is usually required. Investigations are only required to exclude alternative diagnosis.

130
Q

What is the treatment for a migraine?

A

Acute: oral triptan e.g. sumatriptan and NSAIDs e.g. ketoprofen
Prophylaxis - beta blocker e.g. propanolol

131
Q

What are the symptoms of a cluster headache?

A

Recurrent bouts of excruciating unilateral retro-orbital pain, redness or tearing of the eye, nasal congestion, lasts 45-90 minutes and bouts last 6-12 weeks

132
Q

What are the signs of a cluster headache?

A

Eyelid swelling, transient Horner’s syndrome with miosis and ptosis

133
Q

What is the aetiology of trigeminal neuralgia?

A

It is thought to be caused by compression of the trigeminal nerve by a loop of artery or vein; hypertension is a risk factor

134
Q

What is the pathophysiology of trigeminal neuralgia?

A

There is intense and extreme episodes of pain in the face, most commonly the maxillary (V2) and/or mandibular (V3) branch are involved

135
Q

What are the symptoms of trigeminal neuralgia?

A

Preceding symptoms e.g. tingling or numbness, sharp, severe shock like pain on one side of the cheek/face. Pain is episodic and may go into remission.

136
Q

What are some triggers of trigeminal neuralgia?

A

Light touch to the face, eating, cold winds and vibration can all be triggers.

137
Q

What are the signs of trigeminal neuralgia?

A

There are no signs of Vth nerve dysfunction on examination

138
Q

What tests are used to diagnose trigeminal neuralgia?

A

DIagnosis is clinical but can be difficult to make. MRI of the head is indicated to rule out other diagnoses if the diagnosis is uncertain or red flags e.g. deafness, sensory changes are present

139
Q

What is the treatment of trigeminal neuralgia?

A

Medical: carbamazepine, oxcarbazepine
Surgical: microvascular decompression of the trigeminal nerve or rhizotomy - damage the trigeminal nerve to prevent pain transmission

140
Q

What is the aetiology of giant cell arteritis?

A

It is unknown but there are clinical connections with polymyalgia rheumatica, a large vessel vasculitis

141
Q

What is the pathophysiology involved in giant cell arteritis?

A

There is a chronic inflammatory process, predominantly of large arteries. There is systemic immune-mediated vasculitis leading to inflammation of the vessel wall.

142
Q

What are the symptoms of giant cell arteritis?

A

Severe headaches, tenderness of the scalp, jaw claudication and tenderness, diplopia, malaise, tiredness, weight loss, sweats, proximal stiffness (a feature of PMR)

143
Q

What are the signs of giant cell arteritis?

A

Fever, muscle and joints may be tender, bruits (murmur) may be heard over the carotid, axillary or brachial arteries, swelling and tenderness of the temporal or occipital arteries

144
Q

What tests are used to diagnose giant cell arteritis?

A

FBC - normochromic, normocytic anaemia
ESR - high
CRP - high
LFTs - abnormal, high alk phos and low albumin
Biopsy of the temporal artery - granulomatous inflammation of the intima and media, giant cells, lymphocytes and plasma cells in the internal elastic lamina

145
Q

What is the treatment for giant cell arteritis?

A

High dose corticosteroids e.g. IV methylprednisolone
Calcium and vitamin D supplements (+/- bisphosphonates) to prevent osteoporosis
Tocilizumab - anti-interleukin 6 receptor monoclonal antibody

146
Q

What is the aetiology of cauda equina syndrome?

A

Herniation of a lumbar disc (L4/L5 or L5/S1), tumours, trauma, infection, congenital e.g. spina bifida, spondylolisthesis, IVC thrombosis, sarcoidosis, late stage ankylosing spondylitis

147
Q

What is the pathophysiology involved in cauda equina syndrome?

A

There is compression of the nerves forming the cauda equina (L2-S5); it is a MEDICAL EMERGENCY and requires immediate referral

148
Q

What are the symptoms of cauda equina syndrome?

A

Lower back pain, pain in the legs (unilateral or bilateral), lower limb motor weakness and sensory deficits, urinary and/or faecal incontinence, urine retention

149
Q

What are the signs of cauda equina syndrome?

A

Asymmetrical lower limb weakness with loss of reflexes, saddle and perineal anaesthesia, loss of anal tone and sensation, decreased bladder and urethral sensation

150
Q

What tests are used to diagnose cauda equina syndrome?

A

Full history and examination
Emergency MRI of the spine - determine the level of compression
Myelography and CT can be used
Urodynamic studies - monitor the recovery of bladder function

151
Q

What is the treatment for cauda equina syndrome?

A

URGENT NEUROSURGICAL REFERRAL
Immobilise the spine if trauma is the cause
Surgery to remove blood, bone fragments, tumour, herniated disc or abnormal bone growth
Lesion debulking - tumours, abscess
Radiotherapy for malignant causes
Treat the underlying cause e.g. infection or inflammatory disease

152
Q

What is the aetiology of spinal cord compression?

A

Trauma, tumours - benign and malignant, prolapsed disc, epidural and subdural haematoma, inflammatory disease e.g. RA, infection, cervical spondylitic myelopathy

153
Q

What is the pathophysiology involved in spinal cord compression?

A

The pathophysiology is different for each cause but all result in the spinal cord becoming compressed which can lead to irreversible injury

154
Q

What are the symptoms of spinal cord compression?

A

Principal features of chronic and subacute: spastic paraparesis or tetraparesis, radicular pain at the level of compression and sensory loss below the compression

155
Q

What are the signs of spinal cord compression?

A

Tendon reflexes: increase below the level of the injury, absent at the level of the injury and are normal above the injury
Sphincter disturbances, loss of autonomic regulation e.g. lack of sweating

156
Q

What tests are used to diagnose spinal cord compression?

A

Bloods: FBC, U&Es - monitor blood loss and any potential dehydration
MRI of the whole spine
Further investigations depending on the underlying cause

157
Q

What is the treatment of spinal cord compression?

A

URGENT NEUROSURGICAL REFERRAL
Immobilise the spine if trauma is the cause
Surgery to decompress the spine
Lesion debulking
Radiotherapy for malignant causes
Treat the underlying causes e.g. infection

158
Q

What is the aetiology of MS?

A

It is not fully understood, it has a complex polygenic inheritance pattern. EBV and HHV6 may be linked to MS, low vitamin D levels are also linked

159
Q

What is the pathophysiology of MS?

A

It is a T cell mediated autoimmune disease that causes an inflammatory process mainly within the white matter of the brain and spinal cord

160
Q

What are the symptoms of MS?

A

Optic neuritis (impaired vision and eye pain), sensory symptoms, clumsy/useless limb or hand, ataxia, pain, fatigue, bladder and sexual dysfunction

161
Q

What are the signs of MS?

A

Symptoms are worse after heat - Urthoffs
Neck flexion gives an electric shock - Lhermittes
Nystagmus, spasticity

162
Q

What tests are used to diagnose MS?

A

Two or more lesions and one clinical attack disseminated in time and space
MRI head
LP - oligoclonal bands on electrophoresis (not in the seru,)
Visual evoked potentials - delayed p100

163
Q

What is the treatment for MS?

A

Baclofen for spasticity, beta blockers e.g. propranolol for tremor, oxybutynin for urinary incontinence, pain management
Physiotherapy
Acute relapses - steroids
Disease modifying drugs: interferon-beta, glatiramer acetate, natalizumab, alemtuzumab, fingolimod, dimethyl fumarate, terifluromide, mitoxantrone

164
Q

What is the aetiology of myasthenia gravis?

A

It is associated with thymic atrophy or a thymic tumour.

RA, SLE, pernicious anaemia and thyroid disease

165
Q

What is the pathophysiology involved in myasthenia gravis?

A

It is an autoimmune disorder of the NMJ mediated by antibodies to nAChR resulting in depletion of working postsynaptic AChR sites

166
Q

What are the symptoms of myasthenia gravis?

A

Muscle that fatigues more readily after exercise, drooping of the eyelids, slurred speech, nasal sound to the voice

167
Q

What are the signs of myasthenia gravis?

A

Ptosis, diplopia, myasthenic snarl on smiling, peek sign - eyes can’t stay shut for long when forced, tone is normal, sensation is normal, tendon reflexes are normal

168
Q

What tests are used to diagnose myasthenia gravis?

A

Serum anti-AChR and anti-MuSK antibodies, repetitive nerve stimulation and EMG
CT of the thymus - thymoma

169
Q

What is the treatment for myasthenia gravis?

A

Symptom control - anticholinesterase e.g. pyridostigmine
Immunosuppression - prednisolone (give osteoporosis prophylaxis), can also use methotrexate, azathioprine and ciclosporin

170
Q

What is myasthenic crisis?

A

Weakness of the respiratory muscles leading to respiratory failure that can result in intubation and mechanical ventilation.
Treat with plasmapheresis and IV IG

171
Q

What are the types of MND?

A

ALS
Progressive bulbar palsy
Progressive muscular atrophy
Primary lateral sclerosis

172
Q

What is the pathophysiology involved in MND?

A

There is selective loss of neurones in the motor cortex, cranial nerve nuclei and anterior horn cells. It affects both upper and lower motor neurons.

173
Q

What are the symptoms of MND?

A

Limb weakness, wrist drop, foot drop, tendency to trip, slurring of speech, dyspnoea and orthopnoea, sensation of heaviness in one/both legs

174
Q

What are the signs of MND?

A

Muscle wasting, muscle fasciculations, hyporeflexia - LMD

Hypertonia, hyper-reflexia, upgoing plantar responses - UMD

175
Q

What tests are used to diagnose MND?

A

EMG and nerve conduction studies
CT and/or MRI brain and spinal cord - rule out other pathology
Bloods e.g. vitamin B12 levels, folate levels, HIV and Lyme disease serology; creatinine kinase will be increased due to muscle breakdown

176
Q

What is the treatment for MND?

A

Riluzole - sodium channel blocker inhibits glutamate release
Baclofen for spasticity
Amytriptyline for drooling
Analgesia for pain
Palliative care - PEG, non-invasive ventilation, physio

177
Q

What is the aetiology of Guillain-Barre syndrome?

A

Preceding infection, usually of the GI or respiratory tract e.g. EBV, HIV, Campylobacter Jejuni, cytomegalovirus and mycoplasma

178
Q

What is the pathophysiology involved in Guillain-Barre syndrome?

A

The antibodies raised against the preceding infection also attack antigens in the peripheral nerve tissue. It is an ascending and progressive neuropathy

179
Q

What are the symptoms of Guillain-Barre syndrome?

A

Ascending pattern of progressive symmetrical weakness, facial weakness, pain (neuropathic) in the legs and back, sensory loss, reduced sweating

180
Q

What are the signs of Guillain-Barre syndrome?

A

Reduced or absent reflexes, hypotonia, fasciculations, fluctuations of heart rate and arrhythmias, labile blood pressure, variable temperature

181
Q

What tests are used to diagnose Guillain-Barre syndrome?

A

Diagnosis is generally clinical.
U&Es,
LP - increased protein, normal WCC
ECG
Nerve conduction studies
Antibody screen for antibodies against the nerves
Spirometry - assess whether the patient needs an ITU admission

182
Q

What is the treatment for Guillain-Barre syndrome?

A 
Plasmapheresis/plasma exchange
IV IG
VTE prophylaxis e.g. low molecular weight heparin 
Analgesia for pain 
DO NOT GIVE STEROIDS
183
Q

What are some risk factors for carpal tunnel syndrome?

A

Family history, post-Colles’ fracture, DM, thyroid disorders, menopause, acromegaly, renal disease, amyloidosis, pregnancy, obesity

184
Q

What is the pathophysiology involved in carpal tunnel syndrome?

A

There is compression of the median nerve due to increased pressure in the carpal tunnel.
IT IS NOT AN RSI

185
Q

What are the symptoms of carpal tunnel syndrome?

A

Tingling, numbness or pain in the distribution of the median nerve, pain may radiate to the forearm, elbow, arm and shoulder

186
Q

What are the signs of carpal tunnel syndrome?

A

Weakness in hand grip and opposition of the thumb, wasting of the thenar eminence

187
Q

What tests are used to diagnose carpal tunnel syndrome?

A

Phalen’s test - flex the wrist for 60s
Tinel’s test - tapping over the median nerve
Carpal tunnel compression test - apply pressure over the proximal edge of the carpal tunnel
EMG, USS, MRI, electroneurography (ENG)

188
Q

What is the treatment for carpal tunnel syndrome?

A

Conservative: pain relief and a splint at night
Hydrocortisone infection
Surgery: decompression of the nerve

189
Q

What is the aetiology of brain tumours?

A

Primary: astrocytoma (pilocytic astrocytoma to premalignant to anaplastic astrocytoma to GBM) or an oligodendroma (medulloblastoma, lymphoma)
Secondary: lungs > breast > melanoma, renal, GI
Benign: meningioma, neurofibroma

190
Q

What are the symptoms of brain tumours?

A

Headache, nausea and vomiting, diplopia, cognitive or behavioural symptoms

191
Q

What are the signs of brain tumours?

A

Seizures, papilloedema, visual field defects, aphasia, numbness/weakness, cerebellar ataxia

192
Q

What tests are used to diagnose brain tumours?

A

Imaging: CT, MRI, PET scan (to locate primary tumour), CXR
Bloods: FBC, U&Es, CRP, ESR (to rule out other diagnoses e.g. GCA)
Biopsy if possible

193
Q

What is the treatment for brain tumours?

A 
Surgery: resection or debulking
Radiotherapy 
Chemotherapy e.g. temozolomide 
Corticosteroids for cerebral oedema 
Palliative care
194
Q

What are some causes of meningitis?

A

Bacterial: Neisseria meningitidis, Streptococcus pneumoniae, Listeria (elderly), E. coli (neonates)
Viral: Mumps, HSV, poliovirus, echo virus, Coxsackie virus

195
Q

What is the pathophysiology involved in meningitis?

A

There is inflammation of the arachnoid and pia mater, microorganisms infect the CSF. There is pus formation in bacterial infection.

196
Q

What are the symptoms of meningitis?

A

Headache, neck stiffness, leg pains, cold hands and feet, abnormal skin colour, altered mental state

197
Q

What are the signs of meningitis?

A

Fever, photophobia, seizures, non-blanching rash - septicaemia, signs of sepsis
Kernig’s sign - pain and resistance on passive knee extension with the hip fully flexed
Brudzinski’s sign - hips flex when head bends forward

198
Q

What tests are used to diagnose meningitis?

A

Bloods: FBC, U&Es, LFTs, glucose, coagulation, cultures, serology
Swab - throat and rectal
LP - send CSF for MC&S, Gram stain, protein, glucose, virology and lactate

199
Q

What are the common causes of encephalitis?

A

HIV, mumps virus, measles virus, parvoviruses, herpes simplex virus (worst), varicella zoster virus

200
Q

What is the pathophysiology of encephalitis?

A

There is inflammation of the cerebral cortex, white matter, brainstem and basal ganglia

201
Q

What are the symptoms of encephalitis?

A

Headache, altered mental status, seizures, nausea, vertigo, confusion, drowsiness,

202
Q

What are the signs of encephalitis?

A

Fever, photophobia, sensory changes, neck stiffness, focal neurologic signs

203
Q

What tests are used to diagnose encephalitis?

A

Bloods: FBC & film, U&Es, LFTs, glucose, ESR, CRP, cultures
Contrast CT of the head
LP - send CSF for MC&S, viral PCR (increased protein and lymphocytes
EEG

204
Q

What is the treatment for encephalitis?

A

IV aciclovir for 14 days (21 if immunosuppressed)
Supportive therapy
Symptomatic treatment e.g. phenytoin for seizures

205
Q

What is the treatment for meningitis?

A

IV antibiotics cefotaxime +/- ampicillin for Listeria (aciclovir if viral)
ABCDE if necessary
Contact tracing: rifampicin and meningitis C vaccine

Phase 2A (11 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions