Brainscape's Knowledge GenomeTM

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


See full index

Yr4: Neurology & Special Senses > Neurology: Other Less Common Conditions > Flashcards

Neurology: Other Less Common Conditions Flashcards

1
Q

Remind yourself of the following for the cavernous sinus:

  • Location
  • Contents
A

Cavernous sinuses are paired and situated on body of sphenoid bone

Location:

  • Medially: sphenoid sinus & pituitary fossa
  • Laterally: temporal lobe

Contents:

  • Oculomotor nerve
  • Trochlear nerve
  • Ophthalmic division of trigeminal
  • Maxillary division of trigeminal
  • Carotid artery
  • Abducens nerve
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

State some potential causes of cavernous sinus thrombosis

A

Causes can be septic and aseptic:

Septic

  • Sinusitis
  • Facial infection
  • Peri-orbital infection
  • Otitis media
  • Bacterial meningitis
  • Sepsis

Aseptic

  • Trauma
  • Hypercoagulable state
  • Inflammatory disease e.g. SLE
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Describe possible features of cavernous sinus thrombosis

A
  • High fever
  • Headache- particularly around eyes
  • Periorbital oedema
  • Chemosis
  • Cranial nerve palsies & associated double vision
    • CNVI most common (responsible for eye abduction)
    • CNIV (responsible for eye depression, abduction, internal rotation)
    • Ophthalmic division of CNV (absent corneal reflex)
    • Maxillary division of CNV (absent sensation cheek)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Discuss the management of cavernous sinus thrombosis

A

Emergency requiring admission to hospital

  • IV abx
  • Heparin
  • May need surgery to drain if linked to infection
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

State some general/common features of intracranial sinus/venous thrombosis

A
  • Headache (may be sudden onset)
  • Nausea & vomiting
  • Reduced consciousness
  • Cranial nerve palsies
    • Cavernous sinus: CNVI palsy most common
    • Lateral sinus: CNVI and CNVII
  • Can cause cerebral infarction hence present with symptoms & signs of stroke (will depend on region affected)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What is the investigation of choice for intracranial venous thrombosis?

A

MRI venography= gold standard

(CT venography is alternative & according to BMJ actually superior for early detection of cavernous sinus thrombosis. For rest MRI is superior)

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

State some potential causes for brain abscesses

A
  • Recent infection in nearby site (e.g. ear, sinus)
  • Trauma or surgery to scalp
  • Penetrating head injury
  • Embolic events from infective endocarditis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

State some signs & symptoms of a brain abscess

A
  • Signs/symptoms of raised ICP:
    • Headache
    • Nausea & vomiting
    • Seizures
    • Papilloedema
  • Focal neurology
  • Fever
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Briefly outline management of brain abscesses

A
  • Surgery to remove/debride abscess
  • IV antibiotics
  • Dexamethasone to manage increased ICP
  • ?Antiepileptics for seizures
  • ?Antiemetics
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Remind yourself of structure of brachial plexus, include:

  • Roots
  • Trunks
  • Divisions
    *
A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Remind yourself what Erb’s palsy is

A
  • Damage to upper brachial plexus (C5, C6)
  • May be caused in delivery- particularly breech presentation
  • Presentation:
    • Waiters tip (arm adducted, elbow extended, internally rotated, supination, wrist extended)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Remind yourself what Klumpske’s palsy is

A
  • Damage to lower brachial plexus (C8, T1)
  • Usually due to forced hyperextension or hyperabduction (e.g. fall from height and grab onto something) or if baby’s arm is delivered first
  • Claw hand deformity (hyperextension MCPJs, flexion of IPJs, abduction of thumb & wasting of interossei)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

How does a common peroneal nerve injury present?

A
  • Foot drop (MOST COMMON)
  • Others:
    • Weakness dorsiflexion
    • Weakness foot eversion
    • Weakness extensor hallucis longus
    • Sensory loss over dorsum of foot and lower lateral leg
    • Wasting anterior tibial & peroneal muscles

*Remember common peroneal splits into superficial which supplies lateral compartment of leg and deep which supplies anterior compartment of leg

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

Remind yourself of the sensory and motor functions of the median nerve

A

Motor

  • Anterior of forearm
  • Some intrinsic hand muscles (LOAF)
    • Lumbricals 1 & 2
    • Opponens pollicis
    • Abductor pollicis brevis
    • Flexor pollicis brevis

Sensory

  • Palmar aspect of hand (including most lateral 3 and half digits)
  • Distal half of most lateral three & half digits on dorsal aspect of hand
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Discuss how damage to the median nerve at each of the following places would present:

  • Wrist
  • Elbow
  • Anterior interosseous nerve (just below elbow)
A

Wrist

  • Ape hand deformity (flattened thenar eminence, thumb adducted & internally rotated)
  • Due to paralysis and wasting of intrinsic hand muscles supplied by median nerve (LOAF)
  • Palmar cutaneous branch often spared as it exits proximal to the carpal tunnel

Elbow

  • Paralysis of muscles in forearm & arm and sensory loss of lateral palm and lateral dorsal fingertips
  • Presentation:
    • “Hand of benediction” (when make a fist index & middle finger remain extended as lumbricals 1 & 2 supplied by median nerve)
    • Supinated (unopposed action of supinator & biceps brachii)
    • Weak flexion of wrist (can still flex slightly due to flexor carpi ulnaris)
    • Weak or absent flexion of thumb (flexor pollicis longus is paralysed but deep head of flexor pollicis brevis is innervated by ulnar nerve)
    • Sensory loss in median nerve distribution
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Remind yourself of sensory & motor functions of ulnar nerve

A

Motor

  • Flexor carpi ulnaris
  • Flexor half of flexor digitorum profundus
  • Deep head flexor pollicis brevis
  • All muscles in hand except LOAF (lumbricals 1&2, opponens pollicis, abductor pollicis brevis, flexor pollicis brevis superficial head)

Sensory

  • Medial 1 ½ fingers (dorsal & palmar aspect)

*NOTE: palmar cutaneous branch branches proximal to carpal tunnel & guyon’s canal

17
Q

Discuss how damage to the ulnar nerve would present at the:

  • Wrist
  • Elbow
A

Wrist

  • Wasting & paralysis of intrinsic hand muscles
  • Claw hand deformity (hyperextension of MCPJs due to unopposed extension from extensor digitorum, flexion at distal & proximal IPJs due to unopposed flexion from FDS and FDP. Both of the above affect the little & ring finger)
  • Sensation loss in ulnar nerve distribution

Elbow

  • Same as above HOWEVER clawing is less pronounced “ulnar paradox” as the medial half of FDP is paralysed hence not be flexion of DIPJ only hyperextension of MCPJs and flexion of PIPJs
18
Q

Remind yourself of sensory & motor functions of radial nerve

A

Motor

  • Posterior compartments of arm & forearm

Sensory

  • Dorsum of lateral aspect of hand and proximal half of lateral three fingers
19
Q

Discuss how damage to the radial nerve in following places would present:

  • Axilla
  • Wrist
A

Mid-shaft humeral fracture

  • Elbow extension normal or mildly compromised as nerve supply to long & medial head given off prior to radial groove
  • Wrist drop
  • Sensory loss to radially innervated aspects of hand

Axilla

  • Elbow extension would be compromised
  • Same as above PLUS
  • Paralysis of triceps
20
Q

For 3rd nerve palsy, discuss:

  • Presentation
  • Causes
A
  • Presentation:
    • Eye is down & out
    • Ptosis (complete)
    • Dilated pupil (if this occurs called surgical third nerve palsy as suggests not vascular)
  • Causes:
    • Diabetes
    • Vasculitis e.g. GCA, SLE
    • Posterior communicating artery aneurysm
    • Cavernous sinus thrombosis
    • Weber’s syndrome (ipsilateral 3rd nerve palsy with contralateral hemiplegia)
    • False localising sign (due to uncal hernation through tentorium if raised ICP)
21
Q

For a 4th nerve palsy, discuss:

  • Presentation
A

Remember it supplies superior oblique which depresses, extorts and abducts eye.

Presentation:

  • Vertical diplopia (classically noticed when reading a book or going downstairs)
  • May tilt head to compensate or experience tilting of objects
  • Eye may appear deviated upwards and rotated outwards
22
Q

How does a 6th nerve palsy present?

A

Inability to abduct eye on ipsilateral side

23
Q

For Arnold-Chiari malformation, discuss:

  • What it is
  • Features/presentation
A
  • Herniation of cerebellar tonsils through foramen magnum
  • Can be congenital or due to trauma
  • Features:
    • Headache
    • Non-communicating hydrocephalus
    • Syringomyelia
24
Q

Discuss each of the 4 main types of aphasia; for each include where the pathology is and presentation

A

Wernicke’s (receptive) aphasia

  • Lesion in superior temporal gyrus where Wernicke’s area is
  • Speech makes no sense but is fluent. Comprehension abnormal

Broca’s (expressive) aphasia

  • Lesion in inferior frontal gyrus where Broca’s area is
  • Speech is non-fluent, laboured, halting but comprehension is normal

Conductive aphasia

  • Usually due to stroke affecting arcuate fasciculus (connection between Wernicke’s & Broca’s)
  • Speech is fluent but repetition is poor (they are aware of mistakes they are making). Comprehension is normal.

Global aphasia

  • Large lesion affecting all of the above three areas
  • Severe expressive receptive aphasia
  • May still be able to communicate using gestures
25
Q

What are prion diseases?

Briefly outline pathophysiology of prion diseases

A

Prion diseases/transmissible spongiform encephalopathies are a group of rare, progressive, neurodegenerative disorders that affect both humans & animals due to mutated prion proteins forming aggregates and damaging neurones.

  • Prion protein= protein found in cell membranes of neurones thought to have a role in synapses
  • Prion proteins can become misfolded to produce PrPsc (abnormal form of the protein) this may occur due to sporadic mutations, familial inheritance of mutated gene or due to ingestion of PrPsc
  • PrPsc can also cause other normal proteins to misfold
  • PrPsc forms aggregates which destroy neurones and cause brain to have spongiform appearance
26
Q

What is Creutzfeldt-Jakob disease?

How does it present?

A
  • Rapidly progressive neurological condition causes by misfolded prion proteins
  • Rapid onset:
    • Dementia
    • Myoclonus
27
Q

There are 2 types of CJD to be aware of; state and briefly describe each

A

Sporadic CJD

  • 85% cases
  • Mean age onset 65yrs

New variant

  • Younger pts (mean age onset is 25yrs)
  • Psychological symptoms are most common presenting feature
  • Median survival is 13 months
28
Q

What is narcolepsy?

Briefly outline pathophysiology

How does it present?

A
  • Rare long-term brain condition that causes a person to suddenly fall asleep at inappropriate times
  • Associated with low levels of orexin (protein responsible for controlling appetite & sleep patterns)
  • Presentation:
    • Typically starts in teenage years
    • Hypersomnolence
    • Cataplexy
    • Sleep paralysis
    • Vivid hallucinations when going to sleep or waking up
  • Management:
    • Daytime stimulants e.g. modafinil
    • Nightime sodium oxybate
29
Q

What is cataplexy?

What other conditions is it associated with?

A
  • Sudden & transient loss of muscular tone caused by strong emotions (e.g. laughing, being frightened etc…); may range from buckling of knees to collapse
  • ⅔ pts with narcolepsy have cataplexy
30
Q

What is restless leg syndrome?

Describe clinical features

A
  • Syndrome of spontaneous, continuous lower limb movements that may be associated with paraesthesia
  • Features:
    • Uncontrollable urge to move legs (akathisia)- initially at night but may progress to daytime symptoms
    • Paraesthesia (may be described as throbbing or crawling sensation)i
    • Partner may notice periodic limb movements
31
Q

State some potential causes of restless legs syndrome

A
  • FH (50%)
  • Fe deficiency anaemia
  • Uraemia
  • Diabetes mellitus
  • Pregnancy
32
Q

Discuss the management of restless legs syndrome

A
  • Simple/conservative measures: walking, stretching, massaging affected limbs
  • Treat any underlying Fe deficiency
  • First line pharmacological= dopamine agonists (e.g. ropinorole)
  • Others:
    • Benzodiazepines
    • Gabapentin
33
Q

For ataxia telangiectasia, discuss:

  • Inheritance pattern
  • Features
A
  • Autosomal recessive
  • Features:
    • Telangiectasia
    • Cerebellar ataxia
    • IgA deficiency (frequent infections)
    • Increased risk lymphoma & leukaemia
    • Age onset 2-5yrs
34
Q

For Friedreichs ataxia, discuss:

  • Inheritance pattern
  • Features
A
  • Autosomal recessive
  • Features:
    • Cerebellar ataxia
    • Kyphoscoliosis
    • Optic atrophy
    • Diabetes mellitus
    • High arches palate
    • Age onset 10-15yrs
35
Q

For autonomic dysreflexia, discuss:

  • When it occurs
  • Pathophysiology
  • Features
  • Mangement
A
  • Spinal cord injury at or above T6
  • Afferent signals (most commonly triggered by faecal impaction or urinary retention) cause sympathetic spinal reflex via thoracolumbar outflow. The usual, centrally mediated, parasympathetic response is prevented by cord lesion resulting in unbalanced sympathetic physiological response
  • Features:
    • Extreme hypertension (may lead to complications e.g. haemorrhagic stroke)
    • Flushing & sweating above level of cord lesion
    • Agitation
  • Management:
    • Removal/control of stimulus
    • Treatment life-threatening hypertension or bradycardia
36
Q

What is Reye’s syndrome?

State some possible causes

Describe typical presentation

A
  • Severe, progressive encephalopathy in children that is accompanied by fatty infiltration of liver, kidneys and pancreas
  • Aetiology not fully understood but known association with aspirin use and think may be possible viral cause
  • Presentation:
    • Peak incidence 2yrs
    • Hx of viral illness or aspirin use
    • Encephalopathy: confusion, seizures, cerebral oedema, coma
    • Hypoglycaemia

Management is supportive

37
Q

For pituitary apoplexy, discuss:

  • What it is
  • Risk factors
  • Features
A
  • Sudden enlargement of pituitary tumour secondary to haemorrhage or infarction
  • Risk factors:
    • Hypertension
    • Pregnancy
    • Trauma
    • Anticoagulation
  • Features:
    • Sudden onset (similar to SAH)
    • Vomiting
    • Neck stiffness
    • Visual field defects (bitemporal superior quandrantic defect)
    • Extraocular nerve palsies
    • Pituitary insufficiency (E.g. hypotension, hyponatraemia)

Yr4: Neurology & Special Senses (28 decks)

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