Brainscape's Knowledge GenomeTM

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


See full index

Neurology Systems > Week 3 > Flashcards

Week 3 Flashcards

1
Q

what are the names of 3 common cognitive screens?

A
  1. mini mental state examination (MMSE)
  2. montreal cognitive assessment (MOCA)
  3. addenbrooke’s cognitive examination (ACE-III)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

what are the ‘special’ senses and which cranial nerves allow these?

A
  • olfaction (I)
  • vision (II)
  • taste (VII, IX and X)
  • hearing and balance (VIII)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

which cranial nerves are involved with ‘ordinary’ sensation?

A
  • mainly the Vth (trigeminal nerve).
  • the ear from the facial (VII) and (glossopharyngeal (IX) nerves.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

the eye muscles are controlled by which cranial nerves?

A
  • oculomotor III
  • trochlear IV
  • abducens VI
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

the muscles of mastication are controlled by which cranial nerve?

A

V (trigeminal)

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

the muscles of facial expression are controlled by which cranial nerve?

A

facial VII

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

the muscles of the larynx and pharynx are controlled by which cranial nerves?

A

mainly vagus (X) but also glossopharyngeal

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

which cranial nerve controls movement of the SCM and trapezius muscles?

A

accessory (XI)

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

which cranial nerves have autonomic functions (all parasympathetic) and what are the functions?

A
  • oculomotor III > pupillary constriction.
  • facial VII > lacrimation.
  • facial VII > salivation from submandibular and sublingual glands.
  • glossopharyngeal IX > salivation from parotid gland.
  • vagal X input to organs in thorax and abdomen.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

how do we test the function of the optic nerve II?

A
  • visual acuity
  • visual fields
  • pupillary reactions
  • fundoscopy
  • colour vision
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

how do we test the function of the oculomotor, trochlear and abducens cranial nerves?

A
  • any evidence of ptosis?
  • pupil of equal size?
  • pupillar reactions.
  • eye movements > vertical and horizontal.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

how do we test the function of the trigeminal nerve?

A
  • sensation in the opthalamic, maxillary and mandibular regions with e.g. cotton wool.
  • power in muscles of mastication.
  • corneal reflex.
  • jaw jerk.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

how do we test the function of the facial nerve?

A
  • test muscles of facial expression.
  • corneal reflex.
  • taste.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

how do we test the vestibulocochlear nerve function?

A
  • hearing using Rinne’s and Weber’s tests.
  • vestibular function using Dix-Hallpike maneouvre and Utenberger’s test.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

how do we test the function of the glossopharyngeal and vagal nerves?

A
  • movement of the palate
  • gag reflex
  • quality of speech
  • quality of cough
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

how do we test the function of the accessory nerve XI?

A
  • head turning and shoulder shrugging.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

how do we test th function of the hypoglossal nerve?

A

appearance, movement and power of tongue

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

what is the location of the oculomotor and trochlear cranial nerve nuclei?

A

mid brain

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

what is the location of the trigeminal, abducens and facial cranial nerve nuclei?

A

pons

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

what is the location of the vestibulocochlear cranial nerve nuclei?

A

pontomedullary junction

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

what is the location of the glossopharyngeal, vagus, accessory and hypoglossal nerve nuclei?

A

medulla

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

what causes optic neuritis?

A
  • demyelination within the optic nerve.
  • often associated with multiple sclerosis.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

what are the consequences of optic neuritis?

A
  • monocular visual loss
  • pain on eye movement
  • reduced visual acuity
  • reduced colour vision
  • optic disc may be swollen
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

what are some causes of an isolated third nerve palsy?

A

microvascular causes (painless, pupil spared):
- diabetes
- hypertension

compressive causes (painfule, pupil affected):
- posterior communicating artery aneurysm
- raised ICP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

what are some causes of an isolated sixth nerve palsy?

A
  • idiopathic
  • diabetes
  • meningitis
  • raised ICP
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

what causes trigeminal neuralgia?

A
  • caused by compression of trigeminal nerve in the posterior fossa.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

what is the first-line treatment for trigeminal neuralgia?

A

carbamazepine

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

what is dysarthria?

A

disordered articulation
slurring of speech

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

what causes pseudobulbular palsy?

A
  • bilateral UMN lesions of CN IX-XII
  • site > internal capsule
  • MND, MS
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

what causes a bulbar palsy?

A
  • bilateral LMN lesions affecting IX-XII
  • site > medulla
  • MND, polio, tumours, vascular lesions of the medulla, syphilis.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

what are symptoms and signs of bulbar palsy?

A
  • absent/reduced gag reflex
  • wasted, fasciculating tongue
  • jaw jerk absent/normal
  • dysarthria (nasal)
  • dysphagia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

what are symptoms and signs of pseudobulbar palsy?

A
  • exaggerated gag reflex
  • spastic tongue
  • jaw jerk increased
  • spastic dysarthria
  • emotional lability
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

how would you describe a functional neurological disorder?

A

change in function rather than structure of a system (blackouts, paralysis, abnormal movements).

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

what is Hoover’s sign when assessing functional symptoms and signs in neurology?

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

meningitis definition

A
  • inflammation/infection of meninges.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

encephalitis definition

A

inflammation/infection of brain substance

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

myelitis definition

A

inflammation/infection of spinal cord

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

signs and symptoms of meningitis

A
  • headache
  • fever
  • neck stiffness
  • photophobia
  • nausea and vomiting
  • focal neurology
  • seizures
  • reduces conscious level
  • non-blanching petechial rash indicative of sepsis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

what test is used to look for a petechial skin rash in meningitis?

A

Tumbler test

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

what are the organisms responsible for bacterial meningitis?

A
  • Neisseria meningitidis (meningococcus).
  • Streptococcus pneumoniae (pneumococcus).
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

what type of virus can cause meningitis?

A

enteroviruses

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

what are the signs and symptoms of encephalitis?

A
  • fever
  • flu-like prodromal illness (4-10 days)
  • seizures
  • focal neurological deficits
  • headaches
  • cerebral dysfunction: confusion, abnormal behaviour, memory disturbance, depressed concious level)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

how could you perhaps differentiate between viral encephalitis and bacterial meningitis?

A
  • onset of viral encephalitis is generally slower than for bacterial meningitis and cerebral dysfunction is a more prominent feature.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

aetiology of encephalitis

A
  • mainly viral with the most common pathogen being herpes simplex virus type 1 (HSV-1).
  • other viral causes > varicella-zoster virus, epstein-barr virus, cytomegalovirus.
  • meningitis > meningoencephalitis.
  • autoimmune encephalitis.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

what are features of auto-immune encephalitis caused by anti-VGKC (voltage gated potassium channel) antibodies?

A
  • frequenct seizures
  • amnesia (not able to retain new memories)
  • altered mental state
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

anti-NMDA receptor antibodies are a feature of which autoimmune condition?

A

autoimmune encephalitis

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

what are the investigations of meningitis?

A
  • blood cultures (bacteraemia)
  • lumbar puncture (CSF culture/microscopy)
  • no need for imaging if no contraindications to lumbar puncture (CT head if contraindicated).
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

what are the investigations of encephalitis?

A
  • blood cultures and viral PCR
  • imaging (CT scan +/- MRI)
  • lumbar puncture (CSF analysis with viral PCR)
  • EEG
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

what would CSF findings show in bacterial meningitis?

Opening pressure, cell count (and type of WBC raised), glucose, protein

A
  • opening pressure > increased.
  • cell count > high, mainly neutrophils.
  • glucose > reduced.
  • protein > high.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

what would CSF findings show in viral meningitis and encephalitis?

opening pressure, cell count (and type of WBC), glucose, protein

A
  • opening pressure > normal/increased.
  • cell count > high, mainly lymphocytes.
  • glucose > normal (60% of blood glucose).
  • protein > slightly increased.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

aetiology of Arbovirus encephalitides

A
  • transmitted to man by vector (mosquito or tick) from non human host e.g.: West Nile virus.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

describe a brain abscess

A

localised area of pus within the brain

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

what is a subdural empyema?

A

thin layer of pus between the dura and arachnoid membranes over the surface of the brain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

what are the clinical features of brain abscess and empyema?

A
  • fever
  • headaches
  • focal symptoms/signs: seizures, dysphasia, hemiparesis etc.
  • signs of raised intracranial pressure: papilloedema, depressed conscious level.
  • meningism may be present, particulary with empyema.
  • features of underlying source e.g. dental, sinus or ear infection.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

what are some causes of brain abscess and empyema?

A
  • penetrating head injury
  • spread from adjacent infection: dental, sinusitis, otitis media
  • blood-borne infection e.g. bacterial endocarditis
  • neurosurgical procedure
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

how do we diagnose brain abscess and empyema?

A
  • CT or MRI.
  • investigate source.
  • blood cultures.
  • biopsy (drainage of pus).
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

what are the most common organisms responsible for a brain abscess?

A
  • streptococci in 70% of cases, especially the penicillin-sensitive kind: strep anginosus, strep intermedius, strep constellatus.
  • anaerobes in 40-100% of cases: bacteroides, prevotella.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

what is the management for a brain abscess?

A
  • surgical drainage if possible
  • penicillin or ceftriaxone to cover streptococcus (high dosage).
  • metronidazole for anaerobes (high dosage).
  • culture and sensitivity tests on aspirate provide useful guide
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

what are some HIV indicator illnesses affecting the brain?

A
  • cerebral toxoplasmosis
  • aseptic meningitis/encephalitis
  • primary cerebral lymphoma
  • cerebral abscess
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

del

A

del

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

which spirochaetes can infect the CNS?

A
  • lyme disease (Borrelia burgdorferi)
  • syphilis (trepomena pallidum)
  • leptospirosis (leptospira interrogans)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

describe stage 1 of lyme disease

early localised infection (1-30 days)

A
  • early localised infection (1-30 days)
  • characteristic expanding rash at the site of the tick bite: erythema chronicum migrans (circular, target-shaped lesion)
  • 50% flu like symptoms (days-1week): fatigue, myalgia, arthralgia, headache, fever, chills, neck stiffness)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

describe stage 2 of lyme disease

early disseminated disease, lasting from days to months

A
  • early disseminated disease, lasting from days to months
  • continued flu-like symptoms
  • neuroborreliosis: facial nerve and other cranial nerve palsies, aseptic meningitis, encephalitis, peripheral mononeuritis etc.
  • cardiovascular involvement: myocarditis, heart block and other arrhythmias, pericarditis
  • early painful arthritis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

describe stage 3 of lyme disease

late disseminated disease, lasting from months to years

A
  • late disseminated disease, lasting from months to years.
  • arthritis
  • late neurological disorders: polyneuropathy, chronic encephalomyelitis, dementia, psychosis
  • acrdermatitis chronica atrophicans: blue-red discolouration and swelling at extensor surfaces
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

investigations for lyme disease

A
  • complex range of serological tests
  • CSF lymphocytosis
  • MRI brain/spine (if CNS involvement)
  • nerve conduction studies/EMG (if PNS involvement)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

what is the treatment for Lyme disease?

A
  • prolonged antibiotic treatment: IV ceftriaxone, oral doxycycline.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

how is neurosyphilis treated?

A

high-dose penicillin

68
Q

What is a prion disease? Give an example.

A
  • Prion diseases are transmissible, untreatable, and fatal brain diseases of mammals. Their cause is highly unusual: The host’s normal prion protein can, for unknown reasons, malfunction and assemble into structured aggregates called prions that cause infectious brain disease.
  • Creutzfelt-Jakob disease (CJD)
69
Q

signs and symptoms of Creutzfelt-Jakob disease (CJD)

A
  • rapidly progressive dementia
  • neurological symptoms including ataxia, weakness and visual disturbances
  • psychiatric impairment, often preceding the neurological symptoms
  • myoclonus, particulary triggered by startle
70
Q

what is the prognosis of sporadic CJD?

A
  • rapid progression
  • death often within 6 months
71
Q

what is the definition of Brown-Sequard syndrome?

A

characterised by anatomical disruption of nerve fibre tracts in one half of the spinal cord

72
Q

clinical features of Brown-Sequard syndrome?

A

Disruption of descending lateral corticospinal tracts, ascending dorsal column and ascending spinothalamic tracts leads to the following findings below the level of the injury:

  • Ipsilateral hemiplegia
  • Ipsilateral loss of proprioception and vibration
  • Contralateral loss of pain and temperature sensation
73
Q

myelopathy investigations

A
  • localise: imaging- MRI best
  • investigate cause: bloods, CSF
74
Q

which artery is most commonly affected in a spinal cord stroke?

A

usually anterior spinal artery

75
Q

what can cause a vitamin B12 deficiency?

A
  • diet (vegans)
  • pernicious anaemia
  • total gastrectomy
  • Crohn’s disease
  • tape worms
76
Q

symptoms and signs of muscle disease

A
  • weakness of skeletal muscle > respiratory and swallowing muscles important.
  • cardiac symptoms (cardiomyopathy, arrhythmias).
  • cramps/muscle pain, stiffness.
  • myoglobinuria (muscle breakdown product in urine).
  • babies: floppy, poor suckling/feeding/failure to thrive.
77
Q

muscle disease investigations

A
  • history and examination
  • bloods especially creatine kinase (CK)
  • electromyography (EMG)
  • muscle biopsy: structure, biochemistry, inflammation
  • genetic testing
78
Q

what are some congenital/genetic causes of muscle disease?

A
  • contractile: congenital myopathies
  • structural: muscular dystrophies
  • coupling: channelopathies
  • energy: metabolic myopathies
79
Q

what are some acquired causes of muscle disease?

A
  • electrolyte disturbance (especially K+).
  • endocrine: thyroid, adrenal, vitamin D.
  • autoimmune inflammatory muscle disease.
  • iatrogenic: medication (steroids/statins).
80
Q

myasthenia gravis definition

A
  • an autoimmune disease marked by the production of antibodies that target the nicotinic acetylcholine receptors on muscle fibres.
  • reduces the ability of acetylcholine to trigger muscle contraction, resulting in muscle weakness.
81
Q

signs and symptoms of myasthenia gravis

A
  • limb muscle weakness
  • extra-ocular muscle involvement leading to drooping eyelids (bilateral ptosis), diplopia (double vision)
  • facial muscle involvement > difficulty smiling or chewing
  • bulbar muscle involvement > change in speech or difficulty swallowing
  • fatigable muscle weakness, bilateral ptsosis, a myasthenic snarl, head droop, and bulbar features on examination.
82
Q

key investigations in the diagnosis of myasthenia gravis

A
  • blood tests: testing for serum ACh receptor antibody and muscle-specific tyrosine kinase antibodies (anti-MUSK).
  • CT chest to identify thymic hyperplasia or thymoma.
  • nerve conduction studies/EMG: repetitive nerve stimulation testing
83
Q

treatment of myasthenia gravis

A
  • immunosuppressive therapy such as steroids
  • anticholinesterase inhibitors such as pyridostigmine or neostigmine
  • acute cases: IV immunoglovulin or plasmapheresis in severe, steroid-refractory cases
  • thymectomy
84
Q

what are causes of generalised peripheral neuropathy?

A
  • hereditary
  • metabolic: diabetes, alcohol, renal failure, vitamin deficiency
  • toxic: drugs
  • infectious: lyme disease, HIV, leprosy
  • malignancy: paraneoplastic
  • inflammatory (autoimmune), usually demyelinating: acute = Guillain Barre syndrome (post-infectious), chronic = chronic inflammatory demyelinating neuropathy.
85
Q

symptoms and signs of peripheral nerve disease

A
  • loss of sensation, abnormal sensation, pain.
  • muscle thinning, weakness.
  • skin changes, blood pressure, bowel and bladder changes.
86
Q

peripheral nerve disease investigations

A
  • blood tests
  • nerve conduction studies/EMG
  • lumbar puncture (CSF analysis)
  • nerve biopsy
  • genetic analysis
87
Q

motor neuron disease definition

A
  • a group of progressive neurological disorders that destroy motor neurons, the cells that control voluntary muscle activity such as speaking, walking, breathing and swallowing.
88
Q

signs and symptoms of motor neurone disease

A

motor neurone disease typically manifests as a combination of upper and lower motor neurone signs

upper motor neuron signs include:
- spasticity
- hyperreflexia
- upgoing plantars (although they are often downgoing in MND)

lower motor neuron signs include:
- fasciculations
- muscle atrophy

89
Q

motor neurone disease diagnosis

A
  • unique combination UMN and LMN signs, no sensory involvement.
  • electromyography
  • genetic testing
90
Q

what vertebrae is this? and what are its identifying features?

A
  • C1 (atlas)
  • ring-shaped
  • has no body or spinous process but has large transverse processes with foramen transversium accommodating a vertebral artery on either side.
91
Q

what vertebrae is this? what are its identifying features?

A
  • C2 (axis)
  • has body and a distinct 15mm (range 9-21mm) high odontoid process (dens).
92
Q

what vertebrae is this? what are its distinguishing features?

A
  • C7 vertebrae
  • long, non-bifid spinous process
  • transverse foramen and triangular vertebral canal
93
Q

what are some distinguishing features of thoracic vertebrae?

A
  • heart-shaped body
  • small, circular spinal canal
  • presence of costal facets
94
Q

what are distinguishing features of lumbar vertebrae?

A
  • massive kidney-shaped bodies
  • no costal facets
95
Q

how many spinal nerves are there?

A

31 pairs

96
Q

how are the 31 pairs of spinal nerves divided into vertebral levels?

A
  • 8 cervical
  • 12 thoracic
  • 5 lumbar
  • 5 sacral
  • 1 coccygeal
97
Q

sensory info about fine touch, joint position, vibration and proprioception is transmitted via which tract?

A

dorsal column

98
Q

sensory info about pain and temperature is transmitted via which tract?

A

lateral spino-thalamic tract

99
Q

what brain defect occurs due to failure of the anterior neuropore to close during development?

A

anencephaly

100
Q

what birth defect occurs due to failure of the posterior neuropore to close during development?

A

spina bifida

101
Q

what substances obtained from amniocentesis can identify open neural tube defects in high-risk mothers?

A

alpha-fetoprotein (AFP) and acetylcholinesterase

102
Q

describe spina bifida occulta

A
  • incomplete fusion of the vertebrae, but with no herniation of the spinal cord.
  • may be visible only as a small tuft of hair overlying site.
103
Q

describe meningocele spina bifida

A
  • incomplete fusion of the vertebrae, with herniation of a meningeal sac containing CSF.
  • visible prominence at the site, but usually covered by skin.
104
Q

describe myelomeningocele spina bifida

A
  • incomplete fusion of the vertebrae with herniation of a meningeal sac containing CSF and spinal cord.
  • usually accompanied by other defects such as hydrocephaly or Chiari malformation.
  • visible prominence at site, with exposed meninges.
105
Q

clinical manifestations of spina bifida

A

neurological:
- motor deficits
- sensory deficits
- neurogenic bladder or bowel
- hydrocephalus
- seizures

musculoskeletal:
- increased risk of hip subluxation
- scoliosis
- contractures

106
Q

treatment for spina bifida

A
  • primary neurosurgical repair
  • orthopaedic surgery
107
Q

what are the most commonly isolated organisms in pyogenic vertebral osteomyelitis and discitis?

A
  • gram-positive organisms such as Staph.aureus and Streptococcus species.
108
Q

symptoms and signs of pyogenic vertebral osteomyelitis and discitis

A
  • axial pain
  • fever
  • neurological changes: radicular numbness, muscle weakness
109
Q

pyogenic vertebral osteomyelitis and discitis treatment

A
  • administration of broad-spectrum IV antibiotics for at least 6-8 weeks until culture-specific regimens may be initiated.
  • immobilisation may be beneficial for reducing pain and stabilising spine.
  • if needed, surgery: debridement, decompression of neural structures and stabilisation of the spine.
110
Q

how are spinal cord tumours classified?

A
111
Q

what is the gold-standard imaging investigation of spinal cord tumours?

A

MRI

112
Q

best imaging modality for spinal hematomas?

A

MRI

113
Q

treatment of spinal hematomas

A
  • correction of coagulopathy if present, emergency surgical decompression if their is a neurological deficity (usually involves laminectomy).
114
Q

cauda equina syndrome definition

A

a surgical emergency that results from compressive, ischaemic, and/or inflammatory neuropathy of multiple lumbar and sacral nerve roots in the lumbar spinal canal.

115
Q

how does cauda equina syndrome present clinically?

A
  • leg pain, weakness, anaesthesia
  • saddle anaesthesia
  • bladder, bowel and sexual dysfunction
  • decreased anal tone
  • absence of ankle reflex
116
Q

what is the gold-standard imaging modality for cauda equina syndrome?

A

MRI

117
Q

what is the treatment for cauda equina syndrome

A

surgical decompression within 24 hours seems to have best outcomes

118
Q

what is the most commonly affected spinal segment in spinal cord injury?

A

cervical

119
Q

what is the pathology of a primary spinal cord injury?

A

trauma results in the immediate death of local cells:
1. direct damage to cell bodies and/or neuronal processes (die and not replaced)
2. damage to spinal axons (undergoes Wallerian degeneration)

120
Q

pathology of secondary spinal cord injury

A

1) inflammation
2) vascular events: diminished blood flow > ischemia > inflammation and secondary tissue damage
3) chronic pahse of injury which includes: demyelination and scar formation

121
Q

spinal shock definition

A
  • transient loss of all neurologic function below level of the spinal cord injury > flaccid paralysis and areflexia (loss of bulbocavernosus reflex).
  • hypotension
  • duration: 72 hours, but typically persists 1-2 weeks, occasionally several months
122
Q

what can cause spinal shock?

A
  • interrupyion of sympathetics: implies spinal cord injury above T1
  • loss of vascular tone (vasoconstrictors) below level of injury leaves parasympathetics relatively unopposed causing bradycardia
  • relative hypovolemia: skeletal mucle paralysis below level of injury results in venous pooling
  • true hypovolemia: due to blood loss from associated wounds
123
Q

how is resolution of spinal shock firstly recognised?

A

return of bulbocavernosus reflex

124
Q

what are types of incomplete spinal cord injury called?

A
  • central cord syndrome
  • Brown-Sequard syndrome
  • anterior cord syndrome
  • posterior cord syndrome
125
Q

what type of movement is associated with central cord syndrome?

A

usually results from hyperextension injury in older patient with pre-existing stenosis

126
Q

central cord syndrome clinical presentation

A
  • motor: weakness in upper limb more than lower limb
  • sensory: loss below the level of injury
  • sphincter: urine retention
127
Q

what usually causes anterior cord syndrome?

A
  • occlusion of the anterior spinal artery
  • anterior cord compression e.g. by dislocated bone fragment or by traumatic herniated disc
128
Q

clinical presentation of anterior cord syndrome

A
  • paraplegia, or quadraplegia (if higher than C7)
  • dissociated sensory loss below lesion: loss of pain and temperature sensation (spinothalamic tract lesion) with preservation of posterior column function (touch, proprioception, vibration etc.).
129
Q

how does Brown Sequard sydrome manifest?

A
  • ipsilateral loss of joint position sense, vibration sense and discrimination (posterior columns).
  • ipsilateral spastic paresis below the level of lesion (pyramidal tract).
  • contralateral loss of pain and temperature one level below the lesion (lateral spinothalamic tract).
130
Q

multiple sclerosis definition

A

Multiple sclerosis is a chronic autoimmune disease, primarily involving the central nervous system, which is marked by the degeneration of the insulating covers of nerve cells in the brain and spinal cord, leading to demyelination and eventual axonal loss.

131
Q

signs and symptoms of MS

A
  • sensory disease, marked by patchy paraesthesia
  • optic neuritis, characterised by loss of central vision and painful eye movements
  • internuclear opthalmoplegia, a lesion in the medial longitudinal fasciculus of the brainstem
  • subacute cerebellar ataxia
  • spastic paraperesis
  • bladder and bowel involvement
132
Q

pathology of MS

A

Pathologically, CD4-mediated destruction of oligodendroglial cells and a humoral response to myelin binding protein are key features of the disease.

133
Q

classification of MS

A
  • relapsing-remitting (85% at outset)
  • secondary progressive
  • primary progessive (10-15%)
134
Q

discuss the diagnosis of MS

A

based on at least two of:
- clinical history/exam
- imaging findings: typically these are periventricular white matter lesions seen on MRI
- oligoclonal badnds in CSF

135
Q

which criteria are used for an MRI based diagnosis of MS?

A

Posers criteria (clinical)
Macdonald criteria (MRI)

136
Q

acute management of MS

A
  • exclude infection
  • oral prednisolone (intravenous)
  • rehab
  • symptomatic treatment
137
Q

what are symptomatic therapies for MS

A
  • Physiotherapy
  • Baclofen and Botox for spasticity
  • Modafinil and exercise therapy for fatigue
  • Anticholinergics for bladder dysfunction
  • SSRIs for depression
  • Sildenafil for erectile dysfunction
  • Clonazepam for tremor
138
Q

what disease-modifying therapies are used to treat MS?

A
  • First-line injectables such as beta-interferon and glatiramer acetate
  • New oral agents such as dimethyl fumarate, teriflunomide and fingolimod
  • Biologics such as natalizumab and alemtuzumab.
139
Q

what are the three categories of syncope?

A

reflex (neuro-cardiogenic):
- taking blood/medical situations
- cough, micturation

orthostatic:
- dehydration, medication related (anti-hypertensive)
- endocrine, autonomic nervous system

cardiogenic:
- arrhythmia, aortic stenosis

140
Q

epilepsy definition

A

Epilepsy is a neurological disorder characterized by an enduring predisposition to generate epileptic seizures due to abnormal excessive or synchronous neuronal activity in the brain.

141
Q

factors increasing seizure risk

A
  • missed medications (most common)
  • sleep disturbance, fatigue
  • hormonal changes
  • drug/alcohol use, drug interactions
  • stress/anxiety
  • photosensitivity in a small group of patients - other rarer reflex epilepsies (visual patterns, music)
142
Q

how do we classify generalised seizures?

A
  • absence seizures
  • generalised tonic-clonic seizures
  • myoclonic seizures
  • juvenile myoclonic epilepsy
  • atonic seizures
143
Q

how do we classify focal seizures?

A
  • focal seizure with retained awareness
  • focal seizure with loss of awareness
  • focal to bilateral convulsive seizures (secondary generalised)
  • or by location of onset (temporal lobe, frontal etc.)
144
Q

what are features of primary generalised epilepsies?

A
  • no warning before seizure
  • <25 years old
  • may have a histroy of absences and myoclonic jerks as well as GTCS e.g. in juvenile myoclonic epilepsy
  • generalised abnormality on EEG
  • may have a family history
145
Q

what are features of focal/partial epilepsies?

A
  • may get an ‘aura’
  • any age- cause can be any focal brain abnormality
  • simple partial and complex partial seizures can become secondary generalised
  • focal abnormality on EEG
  • MRI may show cause
146
Q

epilepsy investigations

A
  • detailed clinical history and neurological examination
  • electroencephalogram (EEG) for primary generalised epilepsies including hyperventilation and photic stimulation: sometimes sleep deprivation
  • MRI for patients under 50 with possible focal onset seizures
  • CT usually adequate to exclude serious causes >50
  • video-telemetry if uncertain about diagnosis
147
Q

first and second line drugs for status epilepticus?

A
  • first line: lorazepam, midazolam (diazepam)
  • second line: valproate, levetiracetam or phenytoin
148
Q

what drugs are used for primary generalised epilepsies?

A

first line:
- sodium valproate
- levetiracetam
- lamotrigine

second line:
- topiramate
- zonisamide
- clobazam
- (carbamazepine)

149
Q

what drugs are used for focal and focal to bilateral convulsive seizures?

A

lamotrigine
carbamazepine
levetiracetam

150
Q

side effects os sodium valproate

A
  • tremor
  • weight gain
  • ataxia
  • nausea
  • drowsiness (encephalopathy)
  • hepatitis
  • bone marrow suppression
  • drug-induced parkinsonism
  • avoid in women of childbearing age
151
Q

side effects of carbamazepine

A

ataxia
drowsiness
nystagmus
blurred vision
low serum sodium levels
skin rash

152
Q

side effects of lamotrigine

A

skin rash
difficulty sleeping

153
Q

side effects of levetiracetam

A

irratibility
depression

154
Q

describe status epilepticus

A
  • prolonged or recurrent tonic-clonic seizures persisting for more than 30 minutes with no recovery period between seizures.
  • usually occurs in patients with no previous history of epilepsy (stroke, tumour, alcohol).
  • mortality 5-10%
155
Q

what are possible functions of CSF?

A
  • shock absorber for CNS
  • immunological function analogous to lymphatic system
156
Q

what is the production rate and turnover of CSF in adults?

A
  • produced at a rate of about 0.3 ml/min > approx 450ml/24 hours.
  • CSF is turned over 3 times every day.
157
Q

describe a lumbar puncture

A

used to harvest sample of CSF

158
Q

what is hydrocephalus?

A

an abnormal accumulation of cerebrospinal fluid within the ventricles of the brain

159
Q

how can hydrocephalus be categorised?

A

Hydrocephalus can be categorised into non-communicating (obstructive) and communicating types, each with its own causes.
- non-communicating > an obstruction in the ventricular system disrupts the flow of CSF.
- communicating > CSF is not adequately reabsorbed due to damage to the arachnoid villi.

160
Q

what conditions can cause non-communicating (obstructive) hydrocephalus?

A
  • Congenital malformations such as aqueduct stenosis or a Chiari malformation and/or myelomeningocele
  • A tumour or vascular malformation in the posterior fossa
  • An intraventricular haemorrhage (premature infants are particularly at risk)
161
Q

which conditions can cause communicating hydrocephalus?

A
  • Meningitis
  • Subarachnoid haemorrhage
162
Q

signs and symptoms of hydrocephalus in infants

A
  • An enlarged head circumference, noticeable upon inspection or when tracking their growth
  • Bulging of the anterior fontanelle
  • Distention of scalp vein
  • ‘Sunsetting’ of the eyes, a late sign where upward gaze is limited due to raised intracranial pressure
  • irritability, poor head control
163
Q

signs and symptoms of hydrocephalus in older children (with rigid cranial vault) and adults

A

symptoms are those of increased ICP:
- papilledema
- H/A (headache)
- N/V (nausea and vomiting)
- gait changes
- upgaze and/por abducens palsy
- slowly enlarging ventricles may initially be asymptomatic

164
Q

hydrocephalus investigations

A
  • A cranial ultrasound through the anterior fontanelle, typically conducted during the first few months of life when the fontanelle is still open
  • MRI or CT of the brain, offering detailed images to assess ventricular size and identify potential underlying causes such as tumours or haemorrhages
165
Q

hydrocephalus treatment

A
  • lumbar puncture
  • lumbar drain
  • external ventricular drain
  • endoscopic third ventriculostomy
  • ventriculo-peritoneal shunt
166
Q

what is the most likely causative organism in neonatal meningitis?

A

group B streptococcus

167
Q

meningioencephalitis is a complication most commonly associated with which condition?

A

mumps

Neurology Systems (14 decks)

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