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CP3 Medicine > Neurology 1 > Flashcards

Neurology 1 Flashcards

1
Q

What does the anterior cerebral artery supply?

A

Medial surface of the cerebral hemisphere as far back as the peri-occipital sulcus

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2
Q

What does the middle cerebral artery supply?

A

2/3 of the lateral surface of the brain

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3
Q

What do the central middle cerebral arteries supply?

A

Corpus striatum, thalamus and internal capsule

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4
Q

What does the posterior cerebral artery supply?

A

Corpus callosum plus cortex of occipital and temporal lobes

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5
Q

What do the central posterior cerebral artery supply?

A

optic radiation, sub thalamic nucleus and thalamus

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6
Q

What is the blood supply of the brainstem and cerebellum?

A

Vertebral and basilar arteries

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7
Q

What is the function of CNI (Olfactory)

A

Special sensory - smell from the nasal mucosa

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8
Q

What is the function of CNII (Optic)

A

Special sensory - vision from the retina

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9
Q

What is the function of CNIII (Oculomotor)

A

Somatic motor: 4/6 extra-ocular muscles, levator palp superioris

visceral motor: pupil constriction

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10
Q

What is the function of CNIV (trochlear)

A

Somatic motor - superior oblique mm

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11
Q

What is the function of CN V (Trigeminal)

A

Ophthalmic nerve : VI = sensory to superior third of the face and the cornea

V2: sensory to median third of the face and maxilla

V3: sensory - sensation over the mandible and lower lip

MOTOR: muscles of mastication: masseter, pterygoids

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12
Q

What is the function of CNVI (Abducent)

A

Somatic motor: Lateral rectus mm

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13
Q

What is the function of CNVII (facial)

A

Somatic motor: muscles of facial expression
Visceral motor: submandibular/sublingual glands, lacrimal
Special sensory: taste from the anterior 2/3 of the tongue
General sensory: skin of the external acoustic meatus

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14
Q

What is the function of CNVIII? (VC)

A

Special sensory: hearing (vestibular nerve) and balance (cochlear nerve)

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15
Q

What is the function of CN IX (gloss)

A

Somatic motor: stylopharyngeus
Visceral motor: parotid gland
Special sensory: posterior 1/3 of the tongue
general sensory: sensation from the external ear and pharynx
Visceral sensory: visceral feedback from the carotid body

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16
Q

What is the function of CN X (vagus)

A

Somatic motor - palatal / laryngeal / pharyngeal muscles of swallowing

Visceral motor: parasympathetic innervation to smooth muscle of trachea, bronchi, digestive tract and heart

Visceral sensory: same areas as motor

special sensory: taste from the epiglottis / palate

General sensory: sensation from the auricle and external acoustic meatus

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17
Q

What is the function of CNXI (spinal accessory)

A

Motor: SCM, trapezius

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18
Q

What is the function of CNXII (hypoglossal)?

A

Motor: intrinsic / extrinsic muscles of the tongue

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19
Q

Where is the nucleus of CNI?

A

Olfactory epithelium

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20
Q

Where is the nucleus of CNII?

A

Retinal ganglion cells

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21
Q

Where is the nucleus of CN III and IV?

A

Midbrain

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22
Q

Where are the nuclei of CN V, VI and VII?

A

Pons

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23
Q

Where is the nucleus of CN VIII?

A

Vestibular / spiral ganglion

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24
Q

Where is the nucleus of CN IX, X, XII?

A

Medulla

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25
Q

Where is the nucleus of CNXI?

A

Spinal cord

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26
Q

What is bulbar palsy?

A

LMN weakness of muscles supplied by cranial nerves that have their nuclei in the medulla (bulb) CN 9, 10 ad 12

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27
Q

Describe the examination findings of bulbar palsy

A

Tongue: wasted, flaccid and fasiculating, can be moved rapidly

AHH: poor elevation of the soft palate
quiet nasal speech
jaw jerk / gag may be absent

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28
Q

What are the causes of bulbar palsy?

A

Degenerative (MND) or vascular (stroke) most commonly

Inflammatory - GB rarely
infective - botulism
neoplastic - brainstem tumours
congenital

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29
Q

What is pseudo bulbar palsy?

A

Bilateral UMN disease of the medullary cranial nerves

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30
Q

What are the examination findings of pseudobulbar palsy?

A

Tongue: stiff and spastic with slow movements, not wasted
AHH: normal elevation of the soft palate
gravely Donald Duck speech: slurred, high-pitched dysarthria
jaw jerk / gag reflex: preserved, exaggerated jaw jerk

mood disturbances

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31
Q

What are the causes of pseudo bulbar palsy?

A

Degenerative (MND) and vascular (stroke)

Also seen in MS and can follow head trauma

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32
Q

What is the consequence of lesions in the cerebral hemisphere ?

A

Impairment of higher function
‘type’s function affected can give clues as to the location affected, but in reality, if there are localising signs, then cranial imaging will be used to localise the lesion

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33
Q

What are the effects of a frontal lobe lesion?

A

intellectual impairment, personality change, urinary incontinence and mono paresis / hemiparesis

Broca’s aphasia if left frontal area

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34
Q

What are the effects of a left temporo-parietal lesion?

A

agraphia, Alexia, acalculia
wernicke’s (receptive aphasia)
contralateral sensory neglect

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35
Q

What are the effects of a right temporo-parietal lesion?

A

Failure of face recognition

Contralateral sensory neglect

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36
Q

What are the effects of an occipital lesion?

A

Visual field defects, visuospatial defects

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37
Q

Do cerebellar lobes control ipsilateral or contralateral limbs?

A

IPSILATERAL

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38
Q

What is the function of the vermis?

A

Maintains midline posture and balance

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39
Q

Describe lateral cerebellar lesion signs

A 
Broad, ataxic fair
Titubation 
dysarthria
Nystagmus 
dysmetric saccades
upward drift 
rebound phenomenon 
Hypotonia 
Mild hyporeflexia 
Dysmetria 
Dysdiakokinesis
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40
Q

What will midline cerebellar lesions cause?

A

Rolling, broad and ataxic gait
Difficulty standing and sitting unsupported
Cannot perform Romberg’s test with eyes open or closed
Vertigo and vomiting if extension into the fourth ventricle

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41
Q

What are the common causes of bilateral cerebellar dysfunction?

A

Alcohol
drugs: phenytoin, anti-epileptics

Paraneoplastic cerebellar degeneration:
Antineuronal antibodies present
Common with breast cancer and small cell lung cancer

Severe hypothyroidism

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42
Q

What are the common causes of unilateral cerebellar dysfunction?

A

MS
Stroke
Tumour - especially acoustic neuroma, meningioma

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43
Q

What are the structures that make up the basal ganglia?

A

Corpus striatum: caudate nucleus, globus pallidum and putamen

Subthalamic nucleus

Substantia nigra

Parts of the thalamus

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44
Q

What is the function of the basal ganglia?

A

Modulate cortical motor activity

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45
Q

What are the signs of basal ganglia disorders?

A

Bradykinesia
Muscle rigidity
Involuntary movements - tremor, dystonia, athetosis, Chorea, hemiballismus: violent, involuntary movements, restricted to proximal muscles of just one arm

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46
Q

What are the clinical syndromes resulting from basal ganglia pathology?

A

Parkinsonism
Huntingtons
Hemiballismus

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47
Q

What are the causes of central scotoma?

A

Macula lesion: diabetic maculpathy

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48
Q

What is the cause of monocular loss of vision?

A

Ipsilateral optic nerve lesion

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49
Q

What is the cause of bitemporal hemianopia or quadrantanopia?

A

Optic chiasm lesion

50
Q

What is the cause of a superior bitemporal quadrantanopia?

A

Pressure from below the chiasm e.g. pituitary tumour

51
Q

What is the cause of inferior bitemporal quadrantanopia?

A

Pressure from above the chiasm e.g. craniopharyngoma, carotid aneurysm, meningioma

52
Q

What is the cause of a homonymous hemianopia?

A

Contralateral optic tract lesion

53
Q

What is the cause of a homonymous quadrantanopia?

A

Contralateral optic radiation lesion

Temporal lesions give superior homonymous quadrantanopias

Parietal lesions give inferior homonymous hemianopia

PITS

54
Q

What does macular sparing in homonymous hemianopia signify?

A

Defect in the visual cortex: occipital lobe

55
Q

Where is Broca’s area located?

A

Inferior frontal gyrus, areas 44 and 45

56
Q

What is the function of Broca’s area?

A

Motor speech function

57
Q

What is the function of Wernicke’s area?

A

Understanding of the spoken word

58
Q

Where is Wernicke’s area?

A

Superior temporal gyrus - area 22

59
Q

What is Broca’s aphasia?

A

Expressive aphasia:

non-fluent , repetition is poor

60
Q

What is Wernicke’s aphasia?

A

receptive aphasia, loss of ability to understand speech
Fluent: normal production of incorrect words
Poor comprehension: poor repetition

61
Q

What is global aphasia?

A

Both expressive and receptive dysphasia

62
Q

What is nominal aphasia?

A

Difficulty word finding

63
Q

What is dysarthria?

A

disordered articulation / slurred speech, language remains in tact

64
Q

What are the causes of dysarthria?

A

Bulbar palsy
pseudo bulbar palsy
cerebellar lesions
extrapyramidal lesions: soft, indistinct, monotonous speech
myasthenia gravis: Speech fatigues and dies away

65
Q

What is Horner’s syndrome?

A

Oculosympathetic palsy, caused by interruption of the sympathetic chain

Ptosis, miosis and partial anhydrosis

66
Q

What are the symptoms of a Horner’s syndrome?

A

Unilateral pupillary constriction (miosis)
Ptosis
Enophthalmos
anhydrosis

67
Q

What are the causes of a Horner’s syndrome?

A 
First order: 4S:
S – Stroke
S – Multiple Sclerosis
S – Swelling (tumours)
S – Syringomyelia (cyst in the spinal cord)
Pre-ganglionic lesions (4 Ts):
T – Tumour (Pancoast’s tumour)
T – Trauma
T – Thyroidectomy
T – Top rib (a cervical rib growing above the first rib above the clavicle)
Post-ganglionic lesion (4 Cs):
C – Carotid aneurysm
C – Carotid artery dissection
C – Cavernous sinus thrombosis
C – Cluster headache
68
Q

How does the pattern of anhydrosis help to distinguish first-third order disorders?

A

Face/arm/trunk anhydrosis: first order
Facial anhydrosis: second order
No anhydrosis: third order

69
Q

Do LMN innervate ipsilateral or contralateral muscles?

A

ipsilateral

70
Q

Do UMN innervate ipsilateral or contralateral muscles?

A

contralateral

71
Q

Why do lower motor neurone signs occur the way they do?

A

loss of trophic effect on muscles

72
Q

What are the LMN signs?

A 
weakness
wasting
fasciculation 
hypotonia
hyporeflexia
73
Q

Why do UMN signs occur the way they do?

A

Occur due to hyper excitability of inputs to anterior horn cells

74
Q

what are the UMN signs?

A

weakness - extensor weakness in upper limbs and flexor weakness in Lower limbs

no wasting 
hypertonia, spasticity
hyperreflexia
loss of fine motor movement 
pronator drift
extensor plantar response
clonus
75
Q

What are the ddx for LMN lesions?

A

ventral horn pathology - MND, post-polio
peripheral nerve pathology
NMJ pathology
Muscular pathology

76
Q

What are the ddx for UMN lesions?

A 
Vascular: stroke
Inflammatory: MS, MND
Neoplastic: Tumour 
Degenerative: Parkinson's 
Infective: Post-meningitis 
Extra: drugs
77
Q

What is the pyramidal pattern of weakness seen in UMN lesions?

A

Weakness of extensors in upper limbs

weakness of flexors in lower limbs

78
Q

Why is the frontalis spared in UMN lesions?

A

Receives innervation from both U and LMN

79
Q

What are the descending tracts?

A

MOTOR:

Dorsal and ventral CORTICOSPINAL TRACTS

80
Q

are the corticospinal tracts contralateral or ipsilateral?

A

ipsilateral as they decussate in the brainstem

81
Q

What is the function of the corticospinal tract?

A

transmit motor axons from the motor cerebral cortex to the spinal spinal cord

82
Q

What are the ascending tracts?

A 
SENSORY: 
dorsal columns
spinothalamic tract  (lateral and ventral)
83
Q

What is the function of the dorsal columns?

A

Transmit deep touch, joint position and vibration to the parietal cortex

84
Q

Are the dorsal columns ipsilateral or contralateral?

A

ipsilateral - decussate in the brainstem

85
Q

What is the function of the spinothalamic tract?

A

transmits pain, temperature and light touch to the thalamus

86
Q

Is the spinothalamic tract ipsilateral or contralateral?

A

contralateral

decussates at the spinal level

87
Q

What clinical syndrome would arise from a cord transection at C3?

A 
Neurogenic shock 
Respiratory insufficiency 
Quadriplegia
Anaesthesia below the affected level 
Loss of bladder/bowel sphincter tone 
Sexual dysfunction 
Horner's syndrome
88
Q

What clinical syndrome would arise from a cord transection at T10?

A

Paraplegia
Anaesthesia below the affected level
Loss of rectal / bladder sphincter tone
Sexual dysfunction

89
Q

What clinical syndrome would arise from a cord hemisection / BROWN SEQUARD

A

Ipsilateral reduced power (corticospinal tract), vibration and proprioception (posterior or dorsal column)

contralateral reduced pain / temperature and light touch (spinothalamic tract).

90
Q

What is the most common cause of a brown sequard syndrome?

A

Penetrating injury or facet dislocation in a RTA

91
Q

What is the effect of a posterior cord lesion (loss of dorsal tract)

A

tingling, numbness, electric shock like syndrome
clumsiness
on examination: sensory ataxia, loss of positional sense, vibration sense and 2-point discrimination below the level of the lesion

92
Q

what two positions can be used for a lumbar puncture?

A

lying on their side, curled forward with knees up to their chest to open the lumbar interspinous spaces
(lateral recumbent position)
sitting forward curled into a pillow - especially useful in obese patients

N.B. head must be at the same level as the lumbar spine

93
Q

Where is the location of LP?

A

L4
level of the tops of the iliac crest (intercristal plane)

Needle introduced obliquely above L4, parallel to the place of the spine, through the interspinous ligament.

94
Q

What are the indications of LP?

A

Diagnosis of meningitis / encephalitis
Diagnosis of SAH - if clinically suspected but no abnormalities on CT
Measurement of CSF pressure: idiopathic intracranial hypertension

therapeutic removal of CSF - idiopathic intracranial hypertension

Intrathecal drug administration
Diagnosis of misc conditions: e.g. MS, neurosyphilis, Behcet’s disease

95
Q

What are the complications of LP?

A

Post LP headache - occurs in 30%

Dry tap (poor technique)
Infection
Damage to spinal nerves
Coning of the cerebellar tonsils

96
Q

What are the contraindications of LP?

A

Suspicion of mass in the brain / spinal cord or raised ICP
(can lead to coning of the cerebellar tonsils)

Overling / local infection

Congenital lesions in the area

Meningomyelocele

Problems with haemostasis: Platelets <40
Clotting abnormalities
Anticoagulation

Haemodynamic instability

97
Q

Describe the Post LP headache:

A

Occurs in 30% - onset within 24 hours, with resolution over 2 weeks

Classically a constant, bilateral dull ache

Worse when upright due to intracranial hypertension
Treat with analgesics +/- blood patch
Re-injection of a patient’s own blood to form a clot

98
Q

What is xanthocromia?

A

A yellowish colour of CSF

Caused by bilirubin from RBC breakdown

99
Q

What does xanthocromia indicate?

A

That there has been a sub-arachnoid haemorrhage
If the RBCs in the CSF are due to bleeding at the LP site, they will not have been degraded into bilirubin, so CSF will not be xanthocromic

100
Q

What is the ix for suspected SAH?

A

CT within 12 hours of onset (diagnoses 98%)
If there is clinical history of SAH but no CT change - lumbar puncture
Important to detect 2% that cannot be seen on CT: sentinel bleeds from aneurysms present like this and severe bleeds can be fatal

101
Q

What are the CSF findings of MS?

A

moderately raised protein levels: less than 1g/L
Up to 50 lymphocytes/mm3
oligoclonal IgG bands on electrophoresis

102
Q

What are the pros and cons of CT head?

A

pro: rapid procedure - very simple for the patient, good for haemorrhage and calcification
con: Involves ionising radiation

103
Q

What are the pros and cons of MRI head?

A

pros: no ionising radiation and can produce superior anatomical detail in the brain
cons: Longer procedure and many patients cannot tolerate the claustrophobic nature of the scanner

104
Q

What are the contraindications of MRI head?

A

Electrically, magnetically of mechanically activated implants
Pacemakers, cochlear implants, drug infusion pumps

Implants containing ferrous metals: aneurysm clips, surgical staples

Bullets, shrapnel, metal can all move
?Metallic foreign bodies in the eye

Some implants are now made to be safe for MRI scanners

105
Q

What is primary brain injury?

A

Immediate result of a brain trauma

106
Q

What is secondary brain injury?

A

Develop later as a result of complications:
hypoxia
ischaemia
haematomas

107
Q

What is concussion?

A

Transient loss of consciousness but no persistent neurological signs
temporary confusions of amnesia can occur
there may be signs of neurological injury on CT

108
Q

What is diffuse axonal injury?

A

Visible on high resolution CT
number of axons damaged increases with severity of injury
Does not cause raised ICP, and treatment is supportive

109
Q

What are the consequences of diffuse axonal injury?

A

Can cause sequelae of deficiencies in higher function
Loss of concentration / memory disturbances
Personality changes

110
Q

What are focal brain injuries?

A

Gross damage to localised areas of the brain, visible on CT
Coup injuries: beneath the site of impact
Contre-coup: on the opposite side of the brain, due to rebound of the brain within the skull
haemorrhage / haematoma

Can all act as space-occupying lesions and can result in secondary brain injuries

111
Q

What is post-concussion syndrome?

A

dizziness, headache, poor concentration / memory following head injury

inability to work, difficulties with self-care
Physiotherapy and OT may help

112
Q

Describe the steps to examining a patent with head injury

A

C-spine precautions
ABCDE resus

A: guedel airway or intubation usually required
Record GCS prior to intubation

B: chest injuries often co-exist and can lead to secondary brain insults
Hypoxaemia is an indication for intubation

C: polytrauma leading to shock
Cross-match as part of vital bloods

Record GCS
Brief history
?seizures

Neurological exam

Imaging: CT head / C-spine radiography

113
Q

What are the signs of neurological deterioration

A 
Falling GCS - most important sign 
Changing pupillary size / responsiveness 
development of focal neurological signs 
changing respiratory rate 
Falling pulse, rising BP
114
Q

Why does pupil size change in neurological deterioration ?

A

As ICP rises, there is initial progressive dilation on the side of the lesion, and sluggish response to light

This is due to pressure on the oculomotor nerve.
If bilateral, it is a pre-terminal sign

115
Q

What is Cushing’s reflex?

what is it due to?

A

Falling pulse, rising BP
due to pressure on the medulla oblongata
more common in younger patients

116
Q

What is the result of hypercapnia in brain injury?

A

cerebral vasodilation
Increases cerebral blood volume and thus raises ICP

May be hyperventilated on ICU: reduces PaCo2, vasoconstricts cerebral vessels, decreases ICP

117
Q

What is the result of hypoxia in brain injury?

A

can cause cerebral vasodilation

hyperaemia also leads to particularly rapid lactic acidosis within cerebral neurones which causes cerebral damage

118
Q

What is the MAP normally?

What is the effect o head injury on MAP?

A

60-160
auto regulation is lost
cerebral blood Flow relies on SBP
As such, resuscitation is vital to maintain SBP

119
Q

What are the indications for CT after head injury?

1 hour after arrival?

A 
GCS <13 at any time or <15 2 hours after injury 
Focal neurological deficit 
Signs of increasing ICP 
Suspected skull fracture 
Post-traumatic seizure 
Vomiting >1 occasion
120
Q

What are the indications for CT within 8 hours following head injury?

A

Anticoagulated patients
Loss of consciousness plus: Age >65
Dangerous mechanism of injury (e.g. fall from a great height)
retrograde amnesia >30 minutes
Inability to recall the events immediately before injury

121
Q

What are the indications to admit following head injury?

A

If imaging shows pathology
GCS <15
Continuing worrying signs / sources of concern

CP3 Medicine (19 decks)

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