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Neurology Flashcards

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1
Q

What is the function of the frontal lobe?

A

Reasoning, movement, problem solving, behaviour. mood

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2
Q

What is the function of the parietal lobe?

A

Sensory, language functions

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3
Q

What is the function of the temporal lobe?

A

Hearing, memory (contains the hippocampus), understanding speech (wenicke’s areas)

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4
Q

What is the function of the amygdala?

A

Processing and memory of emotional reactions. In the medial temporal lobe.

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5
Q

What structures of the brain help coordinate gross and automatic muscle movement and coordinate muscle tone?

A

Basal ganglia, caudate nucleus, putamen, globus pallidus

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6
Q

What is the role of the epithalamus?

A

Has pineal gland which secretes melatonin (sleepiness and regulates sleep/wake) and habenular nuclei (emotional response to olfaction)

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7
Q

What is the general role of the red nucleus and the substantia niagra?

A

Communicate with the basal ganglia, cerebellum and cerebrum and helps control body movement

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8
Q

What is the role of the hypothalamus?

A

Regulates emotional behaviours and patterns, controls body temperature, eating and drinking behaviour. Controls and integrates activities of the ANS and pituitary gland. Circadian rhythm. Helps in sleep/wake

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9
Q

What is the role of the superior colliculus?

A

Coordinates the movement of the eyeballs in response to visual or other stimuli.
Responsible for lateral upwards gaze

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10
Q

What is the role of the inferior colliculus?

A

Coordinates the movement of the head and trunk in response to auditory stimulus

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11
Q

What is the role of the cerebellum?

A

Smooths and coordinates skilled movement and regulates posture and balance. Involve in muscle tone.

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12
Q

What might a person look like with a CN 3 palsy?

A

Eye in the down and out position. Ptosis, pupil fixed and dilated.

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13
Q

What might a person look like with a CN 4 palsy?

A

Tortional diplopia, compensatory head tilt

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14
Q

What might a person with a CN 6 palsy look like?

A

Eye positioned medially due to reduced abduction of lateral rectus muscle.

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15
Q

What is the function of the brain stem?

A

Controls the flow of messages between the brain and the rest of the body. also controls HR, BP, breathing

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16
Q

Where is broccas area, what is it and what happens if it gets damaged?

A

Inferior frontal gyrus mostly on LEFT
Motor aspect of speech
If damaged - expressive aphasia, non-fluent, slow speech

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17
Q

Where is Wernicke’s area, what is it and what happens if it gets damaged?

A

Superior temporal gyrus - on dominant hemisphere (usually Left)
Understating speech
Damage - Receptive aphasia, extremely poor comprehension

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18
Q

Explain the spinothalamic pathway.

A

Sensory. Pain, crude touch, temperature.
Adelta and c fibres
Noxious stimuli activates free nerve endings which terminate in the dorsal root and synapses with the 2nd order neurone. Here it crosses over via the white commissure to the anterior lateral spinothtalmic tract.
Here it ascends up the spinal cord to the Ventral posteriolateral nucleus of the thalamus. Here it synapses with the 3rd order neurone and ascends through the internal capsule to the primary sensory cortex.

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19
Q

Explain the Dorsal column or medial leminsical pathway.

A

Fine touch, vibration, 2-point discrimination and proprioception.
Abeta fibers
Neurone enters the dorsal Horn and biforcates. One synapses in the dorsal root and the other enters the gracile fasiculus where it ascends up the spinal cord.
It remains on the same side often stimulation.
In the brainstem it synapses in the gracile nucleus and the 2nd order neurone crosses the midline as the internal arcuate fibres. It ascends to the VPL nucleus of the thalamus as the medial lemniscus, where it synapses with the 3rd order neurones and ascends up the internal capsule to the primary sensory cortex

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20
Q

What are some effects of an increased ICP?

A

Headache that is worse in the morning and worse on straining (cough or using the toilet) and stooping
Vomiting
Papilloedema

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21
Q

What are some symptoms of brain herniation?

A

Headache, seizures, loss of consciousness, coma, drowsy, dilated pupil, high BP, loss of reflexes

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22
Q

What is Acute confusional state (delirium)?

A

An acute, fluctuating change in mental status, with inattention, disorganised thinking and altered levels of consciousness. (over Hr-days) EEG abnormal

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23
Q

Give some signs of delirium.

A 
DELIRIUM
Disordered thinking
Euphroia/ emotional liability 
Language impairment
Inattention
Reversal of sleep wake cycles
Illusions and hallucinations 
Unaware/ disorientated
Memory deficits
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24
Q

What are the 4 things a patient must show to be diagnosed with delirium?

A
  1. Change in cognition (memory deficit, disorientated or language disturbance)
  2. A disturbance in attention
  3. Evolves over a short time (hr-days) and is an acute change from baseline and fluctuates throughout the day
  4. Change is evident in the history ± physical exam ± lab findings
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25
Q

What might you see in hyperactive delirium?

A

Heightened arousal, agitation, irritable, hallucinations, inappropriate behaviour

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26
Q

What might you see in hypoactive delirium?

A

Lethargy, lack of interest, reduced motor activity, incoherent speech

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27
Q

What are some possible causes of delirium?

A

PINCHME
Pain
Infection (UTI, penumonia, Line infection, meningitis)
Nutritional (Thaimine or B12 deficiency)
Constipation
Hydration/Hypoxia (rep or cardio failure)
Metabolic (uraemia, electrolyte disturbances, liver failure)
Environment

Alcohol/drug withdrawal
Polypharmacy
Vascular (stroke, MI)

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28
Q

What is motor neurone disease?

A

Progressive degeneration of the motor nueurone cranial nuclei in the motor cortex, anterior horn of the spinal cord and cranial nerve nuclei of the brainstem
Mixed UMN and LMN signs
Weak, clumsy, dysarthria, dysphagia

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29
Q

What are the most common types of MND?

A

Amyotrophic lateral sclerosis - UMN + LMN
Progressive bulbar palsy - dysarthria and dysphagia - UMN
Progressive muscular atrophy - LMN signs

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30
Q

What is Parkinsons disease?

A

A neurodegenerative disease of the basal ganglia in which there is loss of the dopaminergic neurones in the substantia Niagra

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31
Q

Explain how parkinsons may arise

A

Usually symptoms start to bee seen when ~50% of the neurones are destroyed.
The substantia nigra in the midbrain and the corpus striatum in the Basal ganglia communicate via direct and indirect circuits in the niagrostriatal paythway.
Loss of dopaminergic neurones causes increased inhibitory effect on the thalamus which reduced the excitatroy input to the motor cortex

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32
Q

What are some indications of advanced parkinsons disease?

A

Falls, fluctuations in motor activity, sleep disorders, neuropsychiatric disorders

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33
Q

What are some neuropsychiatric symptoms of parkinsons?

A

Dementia, anxiety, depression

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34
Q

What are some autonomic nervous system symptoms of parkinsons?

A

Erectile dysfunction, constipation, urinary urgency, excessive sweating/ salivation, postural hypotension

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35
Q

What drugs might you use in early parkinsons disease?

A

Dopamine agonists. They bind to the dopamine receptors in the post-synaptic membrane.
Ropinirole, Bromocriptine, apomorphine, pramipexole
SE - hallucinations, compulsive behaviour, fainting

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36
Q

What are some side effects of Levodopa drugs for parkinsons?

A

Dyskinesia
Postural hypotension
Confusion, hallucinations

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37
Q

Define depression,

A

A mental state characterised by persistent low mood, lack of interest and enjoyment in everyday activities. A neurovegitative disturbance and reduced energy, causing varying levels of social and occupational dysfunction

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38
Q

How would you diagnose a Major depressive disorder.

A

The presence of at least 5 depressive symptoms. Mild-severe.

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39
Q

How would you diagnose sub threshold (minor) depression?

A

The presence of at least 2-4 symptoms for more than 2 weeks. At leats one of persistent low mood or anhedonia

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40
Q

What is a Persistent depressive disorder (dysthymia)?

A

Characterised by at least 2 years of 3-4 dysthymic symptoms on more days than not

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41
Q

What is Dementia?

A

A chronic, progressive cognitive decline due to brain disease.

  • A deterioration from a higher level of functioning that can’t be explained by normal ageing
  • Chronic >6 months
  • Primarily a CNS disease
  • Not explained by delirium or a major psychiatric disorder
  • Multiple cognitive domains affected involving at least 2 of (Execuative functioning, apraxia/visuospatial, memory)
42
Q

What domains does the addenbrookes cognitive examination assess?

A

Memory, attention, visuospatial ability, language, executive function

43
Q

How might radial nerve damage present?

A

painless Wrist and finger drop
Saturday night palsy, entrapment around the spiral groove
Wrist and finger extension affected

44
Q

What symptoms might you get if you entrap the median nerve in carpal tunnel syndrome?

A

numbness, tingling, nocturnal pain - relieved by shaking
weak grip
Motor - Weak thumb movements

45
Q

What might you get if you entrap the common peroneal nerve at the fibular head

A

Foot drop and sensory changes

Motor- ankle dorsiflexion and great toe extension affected

46
Q

What are some red signs in headaches?

A

SSSNOOPPP
Secondary risk factors, Seizures, Systemic symptoms
Neurological deficit/Sx
Rapid onset, Age onset > 50
Papilloedema, progression (nature, freq,change), Precipitating factors (cough, valsalva, sleep, exercise)

47
Q

Give some characteristics of a tension type headache?

A

Feels like a tight band around the head
Usually at least 10 episodes, <1day/month, <12/year
Bilateral, mild-moderate pain
lasts 30min - 7 days
No N&V, no Photophobia, no aggregated by physic activity

48
Q

Give some characteristics of a migraine headache.

A

A severe headache felt as a unilateral throbbing pain at the front or side of the head
Had prodrome, aura and postdrome.
Headache can last 4 hours - 3 days
moderate - severe pain, pulsatile, unilateral, aggravated or causing avoidance of physical activity
N&V, photophobia or phonophobia

49
Q

What is an Aura?

A

A warning sign of a migraine, usually occurs before the headache, can last from 5min-1hr but usually 20min.
Visual aura- zigzag lines, blind spot, flashing lights
Motor - muscle weakness (one side of body)
Language
Sensory - pins and needles, tingling

50
Q

How might you manage Migraines?

A
  1. Remove trigger - avoid alcohol and caffeine, adequate hydration, regular meals and sleep pattern
  2. Regular analgesia - NSAIDs, Aspirin
  3. PO Triptans (sumatriptan 50-100mg)
  4. If vomiting cyclizine, metaclopromide,prochlorperazine? and SC triptan, SC sumatriptan, SC amlotrpitam, SC Zolmitriptan
51
Q

What is a chronic migraine?

A

> /= 15 headache days per month, of which 8 are migraine days.
Give Onabotulinumtoxin A

52
Q

What is a cluster headache?

A

A series of short, extremely painful headaches every day for weeks or months. Usually seasonal
Severe or very severe unilateral orbital, supraorbital or temporal pain lasting from 15min - 3hr
Unilateral nasal congestion, facial flushing or sweating, miosis, ptosis, fullness in the ear, conjunctival infection.

53
Q

What characterises raised pressure headaches?

A

Worse on lying flat and better when sitting or standing
Worse in the morning
Worse with physical exertion
Persistent N&V
Worse with valsalva manoeuvre (coughing, laughing, straining)

54
Q

What are the complications of SAH?

A 
Haemorrhage 
Delayed ishcaemia
Hydrocephalus
Hyponatraemia 
PE, UTI, Seizures
55
Q

Define seizures?

A

A sustained and synchronised electrical discharge in the brain causing signs and symptoms

56
Q

What is epilepsy?

A

A tendency to have recurrent, unprovoked seizures

57
Q

Define status epilepticus and how you would manage it.

A

Tonic clonic seizures for > 5 min or >/=3 in 1 hour.
A medical emergency
Tx with IV Benzodiazepines

58
Q

What is the MoA of benzodiazepines?

A

Enhance the activity/ binding at the GABA receptor. GABA is the major inhibitory NT in the brain. It inhibits synaptic transmission - sedation, reduced anxiety, sleepiness, anticonvulsant
SE - drowsy, sedation, coma

59
Q

What is a Non-epileptic attack disorder?

A

Due to a temporary problem in the functioning of teh CNS.
Seizure lasts longer than epilepsy
Resistant to eye opening*
Exaggerated movements - pelvic thrust, arched back
Gradual onset can be triggered by anxiety, anger, panic
Rapid recovery

60
Q

What is first line in treating focal seizures?

A

Carbamazepine or lamotrigene

61
Q

What is first line in treating generalised tonic clonic seizures?

A

Sodium valproate

62
Q

What is MS?

A

Idiopathic inflammatory demyelinating disease of the CNS. Discrete plaques of demyelination due to type IV hypersensitivity and cell mediated attack against oligodendrocytes

63
Q

What is Uthoff’s phenomenon?

A

Heat (exercise, infection) makes the symptoms of MS worse

64
Q

What might previous optic neuritis look like?

A

Red desaturation, relative afferent pupillary defect, optic disk pallor, optic atrophy

Painful viusal loss, pain on eye movement, blurring, reduced visual acuity

65
Q

What evidence do you need to diagnose MS?

A

2 or more episodes of demyelination disseminated in space and time

66
Q

What investigations would you do in suspected MS?

A
  1. MRI brain and cervical spine with gadolinium contrast. (Macdonald criteria; at least 2 from; Spinal cord, juxtacortical, infratentorial, periventricular)
  2. LP - Oligoclonal bands in CSF and not in blood after protein electrophoresis
  3. Visual evoked potentials
67
Q

Define a relapse in the context of MS.

A

A new neurological deficit lasting more than 24 hours in the absence of pyrexia or infection

68
Q

Define a pseudo relapse in the context of MS.

A

A re-emergence of a previous neurological deficit relating to an old area of demyelination in the context of pyrexia or infection

69
Q

Natalizumab can be used to treat relapses of MS, what is a risk of taking it?

A

Progressive multifocal leukenchephalopathy due to the JC virus

70
Q

What is first line treatment in relapsing remitting MS?

A
  1. Interferons (beta interferon, glatiramer acetate) dimethyl fumarate
  2. Fingolimod or natalizumab
71
Q

What are the signs that can be seen in a CT at the different Stages after a stroke?

A
  1. Hyperdense vessel sign (90min after onset)
  2. Loss of the insular ribbon (hours)
  3. Hypoattenuation of brain tissue and swelling (24 hours)
  4. Malignant MCA syndrome - rapid neurological deterioration (24hours +)
  5. Encephalomalacia, (chronic, 3 weeks +)
72
Q

Define Stroke.

A

A rapid onset cerebral deficit (usually focal) lasting > 24 hours or leading to death with a vascular cause.

73
Q

What is transient ischaemic attack?

A

A brief episode of neurological dysfunction due to temporary focal cerebral or retinal ishcaemia without infarction, lasts seconds to min with complete recovery. (weak limb. aphasia, loss of vision)

74
Q

How might you manage an ischaemic stroke?

A
  1. A-E assessment
  2. If within 4.5 hours - Thrombolyse with Alteplase IV
  3. If > 4.5hours - Aspirin 300mg PO od 14d
  4. Refer to stroke unit
  5. Endovascular therapy within 6 hours to pull out the clot
75
Q

What symptoms are seen in total anterior circulatory syndrome?

A

Usually proximal MCA or ICA occlusion

Hemiparesis + Hemianopina + higher cortical dysfunction (e.g. aphasia)

76
Q

What is partial anterior circulation syndrome?

A

Usually a branch of MCA occlusion
Isolated higher cortical dysfunction OR 2 of
hemiparesis, hemianopia, higher cortical dysfunction

77
Q

What is posterior circulatory syndrome?

A

Perforating arteries, PCA or cerebellar

Isolated hemianopia or brain stem syndrome

78
Q

What os lacunar syndrome?

A

Perforating arteries, small vessel disease

Pure motor stroke or pure sensory stroke, or sensorimotor stroke, or ataxic hemiparesis

79
Q

What is guillan barre syndrome?

A

Immune mediated demyelination syndrome affecting the peripheral nerves ± spinal roots
often develops weeks after a respiratory or diarrhoea infection - Campylobacter jejuni - trigger causes Ab to attack nerves

80
Q

What is motor neurone disease?

A

Progressive degeneration of the motor neurone cranial nuclei in the motor cortex, anterior horn cell in the spinal cord AND cranial nerve nuclei in the brainstem

81
Q

What bacteria causing meningitis is associated with pigeon droppings?

A

Crytococcal meningitis

82
Q

Where should you take a LP from, what anatomical landmark can help?

A

L3/4

Tufflers line - top of the iliac crests correlates with L3/L4

83
Q

What are some complications of stroke?

A

Seizures, pressure ulcers, aspiration, VTE, haemorrhage transformation, malignant middle cerebral artery syndrome, disability

84
Q

Give some causes of polyneuropathy.

A

B12 def, B6 def, Malignancy, lyme disease, leprosy, HIV, trauma, vasculitis, diabetes, renal disease, GB, nitrofurantoin, alcohol, isoniazid

85
Q

What are the clinical features of Gilliian barre syndrome?

A

Rapidly progressive symmetrical ascending muscle weakness

Distal paresthesia and limb pain

86
Q

What is myasthenia gravis?

A

AI destruction/ blockage of the post-synaptic ACh receptors in the NMJ
Fatiguability of muscles ** Sx worse at end of day or after exercise. NMJ means no sensory Sx
Extraocular muscles affected first - diplopia, ptosis
Anti-ACh receptor Ab in 90%
Paraneoplastic syndrome from a thymoma or thyme hyperplasia so get a CT Thymus
Give AChesterase inhibitors or prednisolone

87
Q

What is Lambert Eaton Syndrome? (NMJ disorder)

A

Impaired neurotransmitter release due to autoantibodies to pre-synaptic voltage gated calcium channels
Often due to small cell lung cancer
Gait problems due to proximal weakness
Dry mouth and constipation, hyporeflexia
IMPROVES after exercise - repeated stimulation eventually leads to enough Ca

88
Q

What is Charcot Marie Tooth?

A

AD sensory and motor neuropathy characterised by symmetrical, distal, slowly progressive muscle wasting
Begins in early adulthood - 20s
Inverted champagne bottle appearance due to distal muscle wasting. also distal sensory loss
Pes cavus, foot drop, claw toes

89
Q

What is muscular dystrophy?

A

Inherited disorders with progressive degeneration of groups of muscles without involvement of the NS
Duchennes MD - X-linked recessive deficit in dystrophin
Symmetrical wasting, weakness and no fasciculation’s or sensory loss

90
Q

Define syncope?

A

TLOC due to global cerebral hypo-perfusion due to hypotension secondary to a fall in CO ± SVR

91
Q

What is L’hermittes sign?

A

An electrical sensation that runs down the back when bending the neck

92
Q

How would you treat an acute relapsing episode of MS?

A

Methylprednisolone

+ PPi

93
Q

In secondary progressive MS a key treatment is controlling sx, what are they?

A

Fatigue - amantadine or modafinil
Urinary Sx - Detrusor hyperreflexia - Oxybutynin or botox. Empyting dysfunction - self catheterise, tamsulosin
Spasticity - PT, OT, benzodiazepins, gabapentin

94
Q

What are some risk factors for delirium?

A 
DELIRIUM
Dehydration
Ears and eyes (sensory impairment)
Limited mobility 
Infection
Really in pain
Impaired cognition 
Up at night 
Medications
95
Q

What are some differentials of delirium?

A 
DELIRIUM
Drugs/dehydration
Electrolyte disturbances
Level of pain
Infection
Resp failure
Impaction of faeces
Urinary retention
Metabolic disorders - liver/renal failure
96
Q

What are some causes of confusion?

A

CHIMPS PHONED
Constipation, hypoxia, infection, metabolic disturbances, Pain, Sleeplessness
Prescriptions, hypothermia/pyrexia, organ dysfunction, nutrition, environmental changes, drugs - illicit, OTC, alcohol

97
Q

List some causes of headaches?

A

VITMAIN CDEF (= sinister causes)
Vascular - SAH, SDH, cerebral venous sinus thrombosis
Iatrogenic - post-LP low pressure headache
Trauma - Traumatic brain injury*
AI - temporal arteritis*
Metabolic - HHS/DKA
Infective - meningitis *
Neoplasm - Brain tumour *
Congenital - AV malformation
Degenerative - temporomandibular dysfunction
Endocrine/ environment - Hunger/hypothyroidism
Functional - stress

98
Q

Raised ICP can cause herniation as the brain tissue tries to moves from an area of high pressure to an area of low pressure. What is uncal herniation?

A

Displacement of the medial temporal lobe (contains uncal and hippocampus) through the incisor of the tentorium.
CN III and posterior cerebral artery can be compressed - ipsilateral dilation. Can also compress motor pathways - weakness, changes in consciousness or coma due to midbrain compression - fixed, dilated pupils, decerebrated posture, resp arrest

99
Q

What type of tremor can be improved by bb or alcohol?

A

Benign essential tremor

Rhythmic, only present when the affected muscle groups are moved

100
Q

What is benign intracranial hypertension associated with?

A

Obesity in young women - Could be talking orlistat (weight loss pill)

101
Q

Weak pincher grip and failure to make the OK sign indicates weakness of what nerve?

A

Anterior interosseous nerve off the median nerve

year 4 (14 decks)

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