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Year 4 > Neurology > Flashcards

Neurology Flashcards

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1
Q

Types of increased tone

A

Spasticity and Rigidity

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2
Q

Difference between spasticity and rigidity

A

In spasticity resistance is different in different directions and is velocity dependent
In rigidity resistance isn’t direction dependent

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3
Q

Spasticity associated with

A

Upper Motor Neuron Lesions

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4
Q

Rigidity associated with

A

Basal Ganglia

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5
Q

Grading Power

A

0 - no muscle contraction seen
1 - flicker of contraction seen, not enough to move the joint
2 - muscle can move if gravity is eliminated
3 - muscle can move the joint with full range but without any resistance
4 - muscle can move the joint against partial resistance
5 - the muscle can move the joint against full resistance

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6
Q

Power 2 =

A

Slight movement with gravity eliminated

Usually a movement parallel to the floor

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7
Q

Power 3 =

A

Movement against gravity

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8
Q

Power 4 =

A

Movement against resistance

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9
Q

Management of Trigeminal Neuralgia

A

Carbamazepine

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10
Q

Preventative Medications in MS (3)

A

Natalizumab
Alemtuzumab
Ocrelizumab

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11
Q

Prophylaxis of Cluster Headaches

A

Verapamil

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12
Q

Management of Cluster Headaches (Acute)

A

High flow oxygen

S/C Sumatriptan

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13
Q

Provocation Procedures in EEG (2)

A
  1. Hyperventilation
    = vigorous breathing results in a transient respiratory alkalosis, causes the constriction of small cerebral blood vessels
    Decreases oxygen supply to the brain
  2. Photic Stimulation
    = stimulation with flashes of light to elicit visual responses in the occipital region
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14
Q

Dysphagia from a neurological cause

A

More likely to be dysphagia to liquids then solids

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15
Q

Examination Findings in Motor Neurone Disease

Finding pattern

A

Fasciculation and brisk reflexes
Pout reflex
Weakness of shoulder abduction
See mixed pattern - combination of UMN and LMN signs. See a LACK of sensory symptoms

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16
Q

Bulbar Palsy =

A

= signs/symptoms occurring due to an impairment of CN IX-XII due to lower motor neurone
Affects muscles of mastication, facial muscles and tongue

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17
Q

Pseudobulbar Palsy =

A

= inability to control facial movements, caused by damage to the corticobulbar pathways
= UMN lesion

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18
Q

Corticobulbar Pathways are

A

The UMN course from the cerebral cortex to the nuclei

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19
Q

Investigation of MND

A

Need MRI, neurophysiology and CK

Usually trying to exclude mimics/other differentials

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20
Q

Drug management in MND

A

Riluzole - prolongs survival

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21
Q

Management in MND

A

SALT and OT
Non-invasive ventilatory support e.g. BiPAP
PEG feeding can be used as long as there isn’t significant bulbar dysfunction

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22
Q

Investigation of choice in suspected SAH

A

Non-contrast CT, under 6 hours of first presentation

Contrast isn’t always of benefit

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23
Q

Preventative medications that can be used in migraine

A

Propranolol
Topiramate
Amitriptyline
Candesartan

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24
Q

Medication to ease vomiting in migraine

A

Prochloperazine

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25
Eye Examination Findings in MS (3)
Pale optic disc on affected side Relative afferent pupillary defect on affected side Reduced visual acuity on affected side
26
Examination Findings in MS (5)
``` Pin and temperature loss on side of weakness Spasticity Weakness of shoulder abduction Brisk reflexes Extensor plantars ```
27
Presentation of GBS (2)
Distal weakness and sensory disturbance | May see areflexia/diminished reflexes
28
Monitoring Requirements in GBS
Vital signs | FVC - GBS can produce a restrictive lung problem
29
What antibodies can be seen in GBS?
Anti-ganglioside antibodies | Seen in up to 60% of GBS cases
30
Management of severe GBS
IV immunoglobulin | Plasma exchange
31
What is CADASIL? Presentation? Genetics?
Hereditary stroke disorder Presentation = migraine with aura, subcortical TIA, progresses to vascular dementia Genetics: mutation of Notch 3 on Ch 19
32
Stiff Person Syndrome Presentation Investigation
= stiffness of axial muscles and superimposed painful spasms | Ix: EMG evidence of continuous motor unit activity, anti-GAD antibodies (tens of thousands)
33
Chronic Inflammatory Demyelinating Polyneuropathy (CIDP)
= neurological disorder characterised by progressive weakness and impaired sensory function Often seeen as the chronic progression of GBS
34
CIDP Pathophysiology Management
Path: damage to the myelin sheath via an unknown autoimmune mechanism Mx: corticosteroids and IV immunoglobulin Physiotherapy may improve muscle strength
35
What are the Parkinson Plus Syndromes?
Multiple System Atrophy Dementia with Lewy Bodies Progressive Supranuclear Palsy Corticobasal Degeneration
36
What areas of the brain are affected in PSP?
Basal ganglia Brainstem (especially the midbrain) Cortex (frontal lobes, limbic system)
37
Presentation of PSP (5)
``` Loss of balance Slowing of movement Impairment of vertical gaze Dementia Pseudobulbar palsy Procerus Sign = characteristic furrowing of the forehead with frowning expression and wide eyed stare ```
38
Presentation of Pseudobulbar Palsy
``` = UMN lesion of CN IX-XII Slow indistinct speech Dysphagia Brisk jaw jerk UMN signs in the limbs ```
39
MRI findings in PSP
Atrophy in the midbrain
40
Differentiating between Parkinson's and PSP
Both have slowed movements and gait difficulty Tremor common in Parkinsons, rare in PSP Abnormal eye movements in PSP, normal in Parkinsons PSP also has a poor response to levodopa
41
Presentation of Multiple System Atrophy (4)
Autonomic Dysfunction e.g. orthostatic hypotension, impotence, dry mouth, urinary retention/incontinence Tremors Slow Movement Muscle Rigidity
42
Types of MSA
MSA-P - parkinsonian features dominate | MSA-C - cerebellar features dominate
43
Neurons degenerated in MSA (3)
Basal ganglia Inferior olivary nucleus Cerebellum
44
Management of MSA
Little levodopa response | Fludrocortisone is useful to prevent orthostatic hypotension
45
Definitive way to diagnose corticobasal degeneration
Neuropathology Examination
46
Presentation of corticobasal degeneration (4)
Parkinsonism Alien Hand Syndrome = unable to control hand movements, feel that the hand is foreign Apraxia Aphasia
47
What are Lewy Bodies?
A-synuclein cytoplasmic inclusions, eosinophillic
48
Presentation of Dementia with Lewy Bodies (4)
Fluctuating cognition Impairments in attention + executive funciton REM sleep disorder Visual hallucinations
49
Investigation of Dementia with Lewy Bodies
SPECT imaging is best
50
Need to avoid using haloperidol in
Dementia with Lewy Bodies | Can cause irreversible Parkinsonism
51
Management of Dementia with Lewy Bodies
Acetylcholinesterase inhibitors | e.g. donsepil, rivastigmine
52
Features of Parkinsonism (4)
Tremor Bradykinesia Rigidity Postural Instability
53
Gait seen in PD
Stooping, shuffling gait
54
Non-Motor Features of PD (3)
Anosmia Depression REM sleep disorder
55
Investigation of PD
Usually clinical diagnosis MRI often normal SPECT imaging can be helpful
56
Management of PD
Levodopa | May use MAO-B inhibitor or dopamine agonist
57
Complication of PD/not taking PD medication
Neuroleptic Malignant Syndrome = high fever, confusion, rigidity, sweating, increased heart rate Can lead to rhabdomyolysis, high K+ and seizures
58
Which drugs block sodium channel influxes in the presynaptic neuron?
Carbamazepine Lamotrigine Phenytoin
59
Which drugs block calcium channel influxes in the presynaptic neuron?
Gabapentin | Pregabalin
60
Which anti-epileptic blocks neurotransmitter release?
Levetiracetam
61
Todd's Paralysis
Post-ictal temporary paralysis
62
Types of Posturing
Decerebrate | Decorticate
63
Management of Partial Seizures
Lamotrigine | Carbamazepine
64
Presentation of Partial Seizures (Motor Fx)
Jerking, posturing, vocalisations
65
Difference between simple and complex partial seizures
``` Simple = no impairment of consciousness, no post-ictal symptoms Complex = impairment of consciousness, may see post-ictal confusion ```
66
Where do complex partial seizures most often originate from?
Temporal lobe
67
Presentation and Investigation of Absence Seizure
< 10 second pauses | See generalised spike wave abnormalities
68
Management of Absence Seizures
Ethosuximide or Sodium Valproate
69
Presentation of Tonic Clonic Seizures (3)
Loss of consciousness Limb stiffening then limb jerking (tonic-clonic) Post-ictal confusion (15 mins - 1 hour)
70
Management of Tonic Clonic Seizures
Sodium valproate | Can offer lamotrigine if SV inappropriate
71
Carbamazepine can make what types of seizure worse?
Myoclonic | Atonic
72
Presentation of Myoclonic Seizures (2)
Sudden jerk of limbs, face and trunk | May see violently disobedient limb
73
Management of Myoclonic Seizures
Sodium Valproate | OR Levetiracetam OR Topiramate
74
Presentation of Atonic Seizures (2)
Sudden loss of muscle tone results in fall | No loss of consciousness
75
Precipitants of Atonic Seizures (4)
Hyponatraemia Infection Head trauma Withdrawal of anti-convulsants
76
Initial drug of choice for Status Epilepticus
Lorazepam 4mg IV
77
Difference between epileptic seizures and functional seizures
Epileptic - eyes are open: won't be able to resist | Functional - eyes shut
78
Management of Spasticity in MS (2)
Baclofen | Gabapentin
79
Investigation of GBS
Use LP | Normal except high protein
80
Extradural bleed VS subdural bleed difference on CT
``` Extradural = limited by the sutures Subdural = not limited ```
81
Acute VS chronic subdural bleed
``` Acute = bright Chronic = hypodense/dark ```
82
Management of MS
Pyridostigmine | The -stigmines are ACh-esterase inhibitors
83
Investigation of choice in MS or demyelinating neuropathy
MRI with contrast | Contrast helps to identify areas of inflammation
84
Meralgia parasthetica =
= entrapment of the lateral femoral cutaneous nerve, results in sensory changes
85
Blood Tests Findings in Neuroleptic Malignant Syndrome (2)
Raised CK Raised WBCs = acute phase response
86
Lacunar infarct =
= can be a pure motor stroke, if so affecting the INTERNAL CAPSULE Arteries e.g. lenticulostriate
87
Bulbar VS Pseudobulbar Palsy
``` Bulbar = LMN lesion of CN IX-XII Pseudobulbar = UMN lesion of CN IX-XII: more common ```

Year 4 (27 decks)

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