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Clinical Medicine > Neuro 2.2 > Flashcards

Neuro 2.2 Flashcards

1
Q

How does TIAs look on imaging?

A

They don’t, fool.

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2
Q

How often do you do the ABCD score?

A

2, 7, and 90 days after CVA

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3
Q

What do you get points for in the ABCD score?

A

 Age > 60 years (1 point)
 BP = 140/90 mmHg at initial evaluation (1 point)
 Speech disturbance without weakness (1 point) OR
 Unilateral weakness (2 point)
 Duration of symptoms of 10-59 minutes (1 point) OR
 Duration of symptoms >60 minutes (2 point)
 DM mellitus in patient’s history (1 point)

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4
Q

ABCD score where hospital observation is unnecessary

A

0-3

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5
Q

ABCD score where hospital observation is justified

A

4-5

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6
Q

ABCD score where hospitalization is worthwhile

A

6-7

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7
Q

If a TIA is probable, what do you do?

A

Apply ABCD score, aspirin, refer to TIA clinic

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8
Q

What does ABCD stand for?

A

age; blood pressure; clinical features of TIA; duration; diabetes

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9
Q

Treatment for patient with TIA and a. fib

A

anticoagulants

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10
Q

Treatment for patients with TIA and mural thrombus

A

anticoagulants

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11
Q

All patients with TIA treatment:

A

ASA
ASA + dipyridamole
Clopidogrel
ASA + clopidogrel

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12
Q

Are anticoagulant drugs recommended in the average patient with a TIA?

A

No

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13
Q

When do you start OAC in patient with TIA and a.fib?

A

1 day after acute event

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14
Q

When do you start OAC in patient with mild stroke and a.fib?

A

3 days after acute event

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15
Q

When do you start OAC in patient with moderate and a.fib?

A

6 days after acute event

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16
Q

When do you start OAC in patient with severe and a.fib?

A

16 days after acute event

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17
Q

Mild stroke NIHSS

A

<8

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18
Q

Moderate stroke NIHSS

A

8-15

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19
Q

Severe stroke NIHSS

A

> 16

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20
Q

Recurrent TIAs with identical clinical features are usually caused by

A

thrombosis or embolism arising from the same site within the cerebral circulation

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21
Q

TIAs that differ in character from event to even suggest ?

A

recurrent emboli from distant or multiple sites

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22
Q

What’s the most common cause of embolic stroke?

A

a. fib

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23
Q

Name five causes of embolic stroke?

A

a. fib; migraine; arterial dissection; temporal arteritis; sickle cell anemia

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24
Q

Name the 5 classic lacunar syndromes

A

pure motor stroke; pure sensory stroke; ataxic hemiparesis; clumsy hand-dysarthria; sensory-motor

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25
Q

Most common classic lacunar syndrome?

A

pure motor

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26
Q

Pure motor stroke

A

hemiparesis affecting the face, arm, and leg to a roughly equal extent, without associated disturbance of sensation, vision, or language- usually located in the contralateral internal capsule or pons

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27
Q

Pure sensory stroke

A

hemisensory loss, which may be associated with paresthesia, and results from lacunar infarction in the contralateral thalamus

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28
Q

Ataxic hemiparesis

A

pure motor hemiparesis is combined with ataxia of the hemiparetic side and usually affects the leg predominantly- results from a lesion in the contralateral pons, internal capsule, or subcortical white matter.

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29
Q

Clumsy hand-dysarthria

A

dysarthria, facial weakness, dysphagia, and mild weakness and clumsiness of the hand on the side of facial involvement

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30
Q

Lacunar strokes occur from?

A

occlusion of small penetrating arteries

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31
Q

The occlusion of what circulation leads to locked-in syndrome?

A

basilar artery, vertebral artery

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32
Q

What is vertebrobasilar insufficiency?

A

poor blood flow to brainstem

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33
Q

Symptoms of vertebrobasilar insufficiency

A

vertiigo with associated neurologic signs; diplopia; ataxia; dysarthria; weakness/paralysis/numbness; drop attacks; HA

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34
Q

What do you need to rule out in any dizziness work up?

A

vertebrobasilar insufficiency

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35
Q

Goal standard for vertebrobasilar insufficiency?

A

Digital subtraction cerebral angiography (DSA)

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36
Q

Two main types of hemorrhagic stroke?

A

ICH and SAH, both of which can lead to IVH

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37
Q

75% of hemorrhagic strokes are due to?

A

ICH

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38
Q

Largest risk factor for intracerebral hemorrhage?

A

HTN

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39
Q

Causes of secondary intracerebral hemorrhage?

A

trauma, arteriovenous malformation, intracranial aneurysm, intracranial neoplasm, cocaine drug exposure

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40
Q

Define intracerebral stroke:

A

acute spontaneous bleeding into brain parenchyma

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41
Q

Primary ICH:

A

results from microscopic small-artery degeneration in the brain, caused by either chronic poorly controlled HTN or amyloid angiopathy

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42
Q

Secondary ICH:

A

intraparenchymal bleeding from a diagnosable anatomic vascular lesion or coagulopathy

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43
Q

ICH: Plasma that is rich in thrombin and other clotting factors then seeps into the surrounding brain tissue, where it triggers a cascade of secondary brain injury that evolves during days to weeks. This unique form of x causes local brain edema, programmed neuronal and glial apoptotic cell death, and breakdown of the brain-blood barrier

A

neurohemoinflammation

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44
Q

The most commonly affected structures in ICH are:

A

basal ganglia and thalamus; lobar regions; brain stem and cerebellum

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45
Q

Cerebral amyloid angiography

A

non-hypertensive lobar intracerebral hemorrhage in the elderly, is characterized by the deposition of B-amyloid protein in small to medium-sized blood vessels of the brain and leptomeninges

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46
Q

Cerebral amyloid angiography CM

A

dementia, gait disturbance, complex partial seizures

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47
Q

CM of ICH:

A

Severe HA, vomiting, BP elevated

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48
Q

Which is more severe ICH or ischemic CVA?

A

neurologic deficit is frequently more severe in ICH

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49
Q

On an non contrast CT, an acute ICH is?

A

hyperdense

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50
Q

On an non contrast CT, a subacute ICH is?

A

isodense

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51
Q

On an non contrast CT, a chronic ICH is?

A

hypodense

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52
Q

Does an ICH get a hospital stay?

A

ICU or stroke unit for at least first 24 hours due to high risk of neurologic deterioration

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53
Q

BP goal of ICH?

A

140 mm HG systolic and MAP of <140 mmHg

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54
Q

In ICH, maintain MAP of <140 mmHg by continuous infusion of?

A

labetalol or nicardipine

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55
Q

In ICH, for elevated INR reverse with?

A

Vitamin K and 4F-PCC

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56
Q

In ICH, for heparin reversal?

A

protamine sulfate

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57
Q

In ICH, for thrombocytopenia or platelet dysfunction?

A

desmopressin and/or transfuse platelets

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58
Q

Expedited INR reversal for life-saving neurosurgical intervention?

A

recombinant activated factor VIIa

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59
Q

How to alleviate intracranial pressure?

A

elevate head of bed to 30 degrees; Mannitol; hyperventilate

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60
Q

Seizure prophylaxis in ICH?

A

fosphenytoin or phenytoin

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61
Q

When is external ventricular drainage indicated in ICH?

A

in all stuporous or comatose patients with intraventricular hemorrhage and ventricular enlargement in whom aggressive support is indicated

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62
Q

In ICH, ICP should be below?

A

20 mmHg

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63
Q

Indications for decompressive posterior fossa surgery in ICH

A

neurologic deterioration, brainstem compression, and hydrocephalus (cerebellar hemorrhage)

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64
Q

Indications for surgical evacuation for lobar hematomas?

A

larger than 30 mL and located approximately 1 cm from brain’s surface

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65
Q

Subarachnoid:

A

caused by rupture of vessels on the brain’s surface, most often due to a congenital aneurysm, and result in diffusion of blood throughout the CSF spaces

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66
Q

Men or Women: subarachnoid?

A

women

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67
Q

Most common cause of SAH?

A

trauma

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68
Q

Most common spontaneous cause of SAH?

A

rupture aneurysms

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69
Q

The thunderclap headache is associated with?

A

SAH

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70
Q

If you suspect a SAH and it doesn’t show up on a non-contrast CT, what do you do?

A

lumbar puncture

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71
Q

What will the CSF look like in a SAH LP?

A

grossly bloody, xanthochromic (yellow-tinged) fluid (present after 12 hours)

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72
Q

Definitive diagnostic procedure to detect intracranial aneurysms and to define their anatomy

A

angiography

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73
Q

SAH BP goal?

A

<160 systolic

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74
Q

BP treatment for SAH?

A

labetalol or nicardipine

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75
Q

Re-bleeding prophylaxis in SAH?

A

e-aminocaproic acid

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76
Q

Seizure prophylaxis in SAH?

A

fosphenytoin or phenytoin

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77
Q

vasospasm prophylaxis in SAH?

A

nimodipine

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78
Q

Cerebral edema treatment in SAH?

A

mannitol or hypertonic saline

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79
Q

ICP goal in SAH?

A

<20 mm Hg

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80
Q

How to diagnosis vasospasm in SAH?

A

transcranial doppler every 1-2 days until the tenth day after SAH; CT angiography and perfusion on day 4-8 after SAH or for neuro worsening

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81
Q

therapy for symptomatic vasospasm in SAH?

A

place patient in trendelenburg; normal saline; if deficit persists, then raise systolic BP with phenylephrine or norepinephrine

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82
Q

If refractory symptomatic vasospasm in SAH, treatment?

A

add dobutamine or milrinone

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83
Q

Definitive treatment for the prevention of re-bleeding in SAH?

A

complete obliteration of a rupture saccular aneurysm by either endovascular coiling or surgical clipping

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84
Q

Procedure that involves packing the rupture aneurysm with platinum coils?

A

endovascular coil embolization

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85
Q

Endovascular coil embolization is good for aneurysms

A

<10 mm in diameter

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86
Q

Surgical clipping requires a craniotomy is preferred for?

A

wide-necked aneurysms

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87
Q

What tool is used to classify SAH?

A

Hunt-Hess Grading Scale

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88
Q

Hunt-Hess Grading Scale: I

A

asymptomatic or mild headaches = 5% hospital mortality

89
Q

Hunt-Hess Grading Scale: II

A

moderate to severe HA or oculomotor palsy = 5% hospital mortality

90
Q

Hunt-Hess Grading Scale: III

A

confused, drowsy, or mild focal signs = 10% hospital mortality

91
Q

Hunt-Hess Grading Scale: IV

A

stupor (localizes to pain) = 34% hospital mortality

92
Q

Hunt-Hess Grading Scale: V

A

coma (posturing or no motor response to pain) = 52% hospital mortality

93
Q

Primary intraventricular:

A

hemorrhage in the ventricular system

94
Q

primary intraventricular hemorrhage is most common in the?

A

occipital horns (lateral ventricles)

95
Q

IVH occurs in x% of the cases of ICH

A

40%

96
Q

What volume of bleed is considered lethal?

A

20 mL

97
Q

Brain vascular malformations

A

space-occupying congenital anomalies that can often exist for a lifetime without symptoms

98
Q

For what is hypertension NOT a risk factor?

A

brain vascular malformations

99
Q

CM of an arteriovenous malformation?

A

most are manifested with intracranial hemorrhage; seizures; or progressive neurologic disability

100
Q

If someone with an arteriovenous malformation develops seizures, what type would they be?

A

focal seizures

101
Q

types of treatment for arteriovenous malformations?

A

selective embolization of the feeding arteries; surgical resection; radiation-induced thrombosis; stereotactic radiosurgery (small lesions)

102
Q

Left (dominant) hemisphere:

A

aphasia, left gaze preference (eyes move toward side of stroke in brain, away from weakness; in a seizure (following a stroke), eyes look away from side of seizure towards weakness); right visual field deficit; right hemiparesis; right hemisensory loss; difficulty reading, writing, or calculating

103
Q

Right (non-dominant) hemisphere:

A

neglect = left hemi-inattention (no comprehension of stroke deficit); right gaze preference; left visual field deficit (neglect); left hemiparesis; left hemisensory loss; bluntness to them—loss of ability to calculate what emotions should be; dysarthria; spatial disorientation; fluent speech, verbal; inability to process anything in left field; apraxia (language is intact, but unable to carry out a motor function; apraxia is the loss of ability to plan movements)

104
Q

subcortical/lacunar:

A

Unilateral symptoms (face, arm, and leg): pure weakness (hemiparesis), pure sensory loss, weakness AND sensory, clumsy/ataxia/dysmetria (subtle weakness with clumsiness), dysarthria clumsy hand; alert, oriented, following commands; no aphasia

105
Q

Brainstem infarct symptoms: basilar artery

A

Hemiparesis (sometimes quadraparesis); crossed sensory signs; diplopia, disconjugate gaze, gaze palsy, nystagmus; vertigo, tinnitus; dysarthria; N/V; hiccups, abnormal respirations; decreased consciousness

106
Q

Frontal lobe infarct

A

difficulties with attention, uncontrolled emotional, social, and sexual behavior changes, personality changes, loss of spontaneity, problem-solving difficulties, perseveration, loss of verbal expression, difficulty sequencing, inflexible thinking

107
Q

Parietal lobe infarct

A

reading and writing problems; object naming problems; right/left confusion; math difficulties; inability to focus visual attention; problems with eye-hand coordination; lack of awareness of body parts

108
Q

temporal lobe infarct

A

difficulty understanding spoken words, disturbance of selective attention, short-term memory loss, change in sexuality, persistent talking, increased aggressive behavior, difficult identifying and categorizing objects, difficulty recognizing faces and visually locating objects

109
Q

occipital lobe infarct

A

vision defects (visual field cuts), difficulty visually locating objects, difficulty identifying colors, hallucinations and visual distortions, word blindness, inability to recognize object movement, difficulties reading and writing

110
Q

cerebellum infarct

A

decreased breathing capacity; difficulty swallowing food and fluid; problems with balance and movement; dizziness and nausea; vertigo; sleeping difficulties

111
Q

What tool is used to measure stroke?

A

NIHSS

112
Q

NIHSS score greater than or equal to X has a 91% predictive positive value for a central large-vessel stroke

A

12

113
Q

NIHSS greater than x indicates a more proximal vessel affected

A

> 10

114
Q

Cincinnati Pre-Hospital Stroke Scale

A

facial droop; arm drift (ten seconds); abnormal speech (“you can’t teach an old dog new tricks”)

115
Q

If any one of the cincinnati pre-hospital stroke scales is positive, then the probability of a stroke is?

A

72%

116
Q

a non-contrast CT scan has high sensitivity for?

A

detection of hemorrhage

117
Q

a non-contrast CT scan is insensitive for?

A

lacunar and posterior fossa strokes

118
Q

What does a perfusion scan show?

A

what tissue is already infarcted and what tissue is at risk

119
Q

A stroke brain volume of X is likely a good outcome

A

<50 mL

120
Q

On a CT scan, an ischemic stroke will be?

A

hypodense

121
Q

On a CT scan, a bleeding stroke will be?

A

hyperdense

122
Q

MRI is sensitive to?

A

acute ischemia; posterior fossa; small vessel/lacunar strokes

123
Q

Three tests to assess embolic source of stroke?

A

TTE; TEE; telemetry

124
Q

Goal standard echo for stroke?

A

TEE

125
Q

family/essential tremor genetics?

A

AD

126
Q

patho of family/essential tremor?

A

microscopic abnormalities of cerebellar Purkinje cells

127
Q

Patients with essential tremor have a higher risk of developing?

A

Parkinson disease

128
Q

what provides transient relief to those with essential tremor?

A

alcohol

129
Q

First line treatment of essential tremor?

A

propranolol; primidone; topiramate

130
Q

Chorea patho?

A

cell loss in the caudate nucleus and putamen

131
Q

Sydenham chorea patho?

A

immunologic cross-reactivity between the causative group A B-hemolytic streptococcus and the basal ganglia; late component of rheumatic fever

132
Q

Five causes of chorea?

A

HD, Wilson, drug toxicity, Addison, HIV

133
Q

Treatment of chorea in adults?

A

haloperidol and pimozide

134
Q

Treatment of chorea in children?

A

clonazepam, diazepam, clobazam; valproate

135
Q

drug of choice in Sydenham chorea?

A

valproate and short term abx

136
Q

Ballism

A

extreme form of chorea

137
Q

Ballism cause?

A

most often a consequence of an acute cerebral insult such as a stroke (normally one side of body– hemiballism)

138
Q

Hemiballism cause?

A

vascular disease in the contralateral subthalamic nucleus

139
Q

HD patho?

A

atrophy of the caudate nucleus and to the less degree the putamen and globus pallidus

140
Q

Symptom onset of HD?

A

30-55 years

141
Q

Diagnosis of HD?

A

CT/MRI; PET; genetic testing

142
Q

Treatment of HD: movement

A

reserpine, tetrabenazine, haldol, quetiapine

143
Q

Treatment of HD: psychosis

A

olanzapine or risperidone; quetiapine

144
Q

Dystonia

A

sustained muscle contractions result in repetitive twisting and sometimes tremulous movements and abnormal postures

145
Q

Name for twisting neck to one side

A

torticollis

146
Q

name for spontaneous, involuntary forced closure of eyelids; difficulty in eye opening; repetitive blinking

A

blepharosams

147
Q

name for spasms of the muscles of the mouth

A

oromandibular dystonia

148
Q

Slower, sinuous writhing dystonic movements, particularly present in the distal limbs:

A

athetosis

149
Q

Dystonia is often made worse by?

A

activity

150
Q

First line treatment of dystonia:

A

focal injections of botulinum

151
Q

Medications for dystonia:

A

trihexyphenidyl (anticholinergic), diazepam, tetrabenazine (dopamine depleting), haldol (dopamine blocking

152
Q

medication treatments for tics

A

haldol, pimozide, risperidone

153
Q

CM of Tourette’s

A

Presence of multiple motor and at least one vocal tic beginning before the age of 21 years (typically between ages 2 and 10 years) and lasting for more than 1 year, waxing and waning symptoms over time (new tics replacing old ones; previous tics sometimes recurring years after they had originally resolved), and the absence of other explanatory medical conditions

154
Q

treatment for moderate Tourette’s

A

low-dose clonazepam, clonidine, guanfacine, risperdal, apiprazole, botox

155
Q

Are motor tics or vocal tics more common as an initial presentation of Tourette’s

A

motor

156
Q

involuntary swearing

A

coprolalia

157
Q

Myoclonus

A

Sudden, brief, shock-like, involuntary movements that result from both active muscle contraction (positive myoclonic jerks) and brief inhibition of ongoing muscle activity (negative myoclonic jerks)

158
Q

Most common myoclonus

A

asterixis

159
Q

Myoclonic jerks typically last?

A

<150 msec

160
Q

Treatment of myoclonus?

A

clonazepam, valproic acid, carbamazepine, levetiracetam

161
Q

Restless leg syndrome inheritance

A

AD

162
Q

80% of patients with restless leg syndrome have an associated movement disorder called

A

nocturnal myoclonus

163
Q

Treatment of restless leg syndrome

A

pramipexole, ropinirole, transdermal rotigotine; gabapentin, L dopa

164
Q

Parkinson disease patho:

A

due to loss of dopamine in the neostriatum (especially in putamen) secondary to loss of pigmented dopaminergic neurons in the substantia nigra of the midbrain

165
Q

Four cardinal signs of Parkinson

A

tremor, rigidity, akinesia, and postural disturbances (TRAP)

166
Q

Five causes of secondary parkinson?

A

dementia with lewy bodies, AD, wilson, CJD, MS

167
Q

AD Parkinson genes

A

a-synuclein gene mutations, duplications, triplications; LRRK2

168
Q

AR Parkinson genes

A

parkin, DJ1, PINK1

169
Q

what occurs in the substantia nigra of Parkinson

A

cell loss, gliosis, abnormal deposition of aggregated a-synuclein as Lew bodies and Lew neutrites

170
Q

What’s the classic symptom of Parkinson’s?

A

resting tremor

171
Q

Describe the resting tremor in PD?

A

4-6 cycles per second; typically with “pill-rolling” character when it involves the hand

172
Q

Muscle rigidity in PD can be most appreciated ?

A

slow passive movements

173
Q

Muscle rigidity in PD can be classified as x when a tremor is superimposed

A

cogwheel

174
Q

Muscle rigidity in PD can be classified as x when the tremor is not superimposed

A

lead pipe

175
Q

masked facies AKA (in PD)

A

hypomimia

176
Q

soft monotonous speech (in PD)

A

hypophonia

177
Q

impaired swallowing resulting in drooling ( in PD)

A

sialorrhea

178
Q

small handwriting (in PD)

A

micrographia

179
Q

postural disturbances in PD

A

flexed posture in the limbs and trunk (stooped, simian posture), postural instability

180
Q

Multiple system atrophy: CM

A

early dysautonomia and bladder dysfunction; cerebellar dysfunction

181
Q

MSA-P CM

A

pyramidal tract signs; stimulus-sensitive myoclonus of hands and face

182
Q

MSA-C CM

A

extreme forward neck flexion; mottled, cold hands; inspiratory stridor; prominent dysarthria

183
Q

progressive supranuclear palsy CM

A

supranuclear vertical ophthalmoplegia; ocular and eyelid disturbances; axial rigidity > limb rigidity; early falls; speech and swallowing disturbances; nuchal extension; cognitive or behavioral changes; progressive nonfluent aphasia; HTN

184
Q

Corticobasal degeneration CM

A

apraxia, cortical sensory loss, alien limb phenomenon; pronounced asymmetrical rigidity; limb dystonia; stimulus-sensitive myoclonus; aphasia; cognitive dysfunction

185
Q

What condition shows a “hot cross bun sign” on MRI

A

MSA-P

186
Q

What condition shows a hummingbird sign on midline sagittal view?

A

progressive supranuclear palsy

187
Q

What condition shows a morning glory sign on axial view?

A

progressive supranuclear palsy

188
Q

Vascular parkinsonism Cm

A

lower half parkinsonism with gait disturbances predominating

189
Q

What’s considered lower half parkinsonism?

A

vascular parkinsonism and normal-pressure hydrocephalus

190
Q

Parkinson imaging

A

PET scan

191
Q

Group A features of Parkinson

A

resting tremor, bradykinesia, rigidity, asymmetric onset

192
Q

PD drugs used early on:

A

anticholinergics; amantadine; MAO-B inhibitors

193
Q

anticholinergics used in PD

A

benztropine; trihexyphenidyl

194
Q

MAO-B inhibitors used in PD

A

selegiline, rasagiline

195
Q

drugs used later in PD?

A

dopamine agonists

196
Q

what drugs are more helpful in alleviating tremor and rigidity in PD?

A

muscarinic anticholinergics

197
Q

MOA for anticholinergic drugs

A

blockade of NMDA-preferring glutamate and muscarinic cholinergic receptors and stimulation of dopamine release

198
Q

Amantadine improve?

A

all motor symptoms of PD; reducing intense fatigue; iatrogenic dyskinesias

199
Q

Issue with Amantadine?

A

short lived

200
Q

Potential first line treatment for PD?

A

amantadine

201
Q

Most effective treatment of PD?

A

levodopa

202
Q

levodopa is converted in the body to

A

dopamine

203
Q

What drug can be given with levodopa to limit the breakdown of levodopa outside the brain?

A

carbidopa

204
Q

Carbidopa inhibits?

A

dopa decarboxylase

205
Q

Levodopa SE

A

nausea, vomiting, hypotension, abnormal movements, restlessness, confusion; cardiac arrhythmias

206
Q

dopamine agonists used in PD

A

bromocriptine, pramipexole, ropinirole, apomorphine

207
Q

which two dopamine agonists can be used in early PD?

A

pramipexole/ropinirole

208
Q

Pramipexole/ropinirole AE

A

fatigue, somnolence, nausea, peripheral edema, dyskinesias, confusion, hallucinations, orthostatic hypotension; sleep at inappropriate times; disturbances of impulse control

209
Q

Apomorphine may help resuce patients with?

A

advanced PD and severe “off” episodes of akinesia despite optimized oral therapy

210
Q

Apomorphine AE

A

severe nausea, vomiting, somnolence, hallucinations, chest pain, hyperhidrosis, dyskinesias may be enhanced

211
Q

monoamine oxidase B inhibitors used in PD

A

selegiline and rasagiline

212
Q

MO and COMT are enzymes that break down?

A

dopamine

213
Q

Selegiline MOI

A

inhibits the metabolic breakdown of dopamine and enhances the antiparkinsonian effect of levodopa and may reduce mild on-off fluctuations in responsiveness

214
Q

Rasagiline

A

effective in the initial treatment of early PD; more potent and selective the selegiline

215
Q

catechol-o-methyltransferase inhibitors used in PD

A

entacapone, tolcapone

216
Q

COMT drugs may be used for?

A

reduce the dose requirements and any response fluctuations to levodopa; more sustained plasma levels of levodopa with improved transport into the blood and across BBB

217
Q

SE of COMT drugs

A

diarrhea, confusion, dyskinesias, abnormalities of liver tests

218
Q

What alternative treatment may be used in PD?

A

deep brain stimulation

219
Q

gait disturbances and akinesia may be helped in PD by stimulation of

A

the pedunculopontine nucleus

Clinical Medicine (13 decks)

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