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Neurology Flashcards

1
Q

One pupil is dilated and nonreactive to light or accommodation

A

Hutchinson pupil

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2
Q

UMN lesions affect what areas of the nervous system?

A

The brain or the spinal cord

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3
Q

What is the presentation of UMN lesion?

A

Increased muscle tone, increased reflexes, babinski is positive, pronator drift positive

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4
Q

What is the next step in diagnosis if you suspect a patient has an UMN lesion?

A

CT or MRI

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5
Q

Why does a patient with an UMN lesion have sparing of the Upper face?

A

Remember that the upper motor neurons synapse at both an upper and lower nucleus. The upper nuclei supplies the upper half of the face while the lower nuclei supplies the lower half. Keep in mind there is colateral innervation from the oppisite side of the cortex that suplies the neuron, meaning that the upper part of the face is innervated.

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6
Q

Lesion of the ____ motor neuron results in complete paralysis of one side of the face, resulting in an inability to close the eyes, smile, and decreased labial folds

A

LMN

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7
Q

A sensitive test for UMN lesion. Patients are asked to extend their hands with their palm up and close their eyes.

A

Pronator drift, if the patients palms rotate downward this is a positive sign.

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8
Q

What are the signs of LMN lesion?

A

Flaccidity, hyporeflexia, atrophy, fibrillation (small contractions detected on EMG) fasciculations (larger contractions)

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9
Q

What are etiologies for Bell’s palsy?

A

Herpes simplex, lyme, sarcoidosis

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10
Q

The inability to perform a series of rapidly alternating movements. Ask the patient to keep one hand over the other and rapidly move the upper hand in alternating supination/pronation.

A

Dysdiadokinesia

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11
Q

The patient overshoots when attempting to reach something

A

Dysmetria

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12
Q

Slurred speech

A

dysarthria

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13
Q

Signs that the cerebellum may be damaged?

A

DANISH Pendulum; dysdiadokinesia, dysarthria, ataxia, nystagmus, intention tremor, slurred speech, hypotonia, persistent back and forth swinging of the leg

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14
Q

What is the next step in managment if you suspect a patient has cerbellar comprimise?

A

CT or MRI

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15
Q

A 53 yo pt suddenly has painless loss of vision (like a “dark curtain” over one eye) followed by spontaneous recovery. What is the Dx?

A

Amaurosis fugax, which affects the retinal branch of the internal carotid artery

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16
Q

A 50 yo F patient woke up with symptoms of difficulty speaking and weakness in his right leg that lasted for 3 hours. Patient is currently asymptomatic. What is the next step in managment?

A

Aspirin, statin, Patient should also get a carotid duplex to see if intervention is required.

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17
Q

Where do the vertebral arteries originate from?

A

The subclavian artery

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18
Q

What branches does the basilar artery give off?

A

Pontine

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19
Q

The basilar artery eventually gives rise to what first portion to the circle of Willis?

A

The posterior cerebral artery

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20
Q

This artery of the brain gives off the lenticulostriate arteries

A

MCA

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21
Q

Where is the stroke happening in a patient where the upper extremities, and face are affected, homonymous hemianopia (it is contralateral)

A

MCA

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22
Q

Branches off of the MCA, supply what deeper structures of the brain?

A

The Internal capsule, thalamus, basal ganglia and temporal lobe.

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23
Q

A patient with MCA in the right lobe of the brain will have these additional signs associated with speech?

A

Broca and Wernicke’s

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24
Q

A patient with MCA in the left lobe of the brain will have these additional signs?

A

Hemineglect, constitutional apraxia where the can understand what’s going but cannot execute the task

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25
Q

CN I

A

olfactory

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26
Q

CN II

A

Optic

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27
Q

CN III

A

Oculomotor which controls all the eye muscles except for the SO, and the lateral rectus

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28
Q

CN IV

A

Trochlear (supplies the SO), superior is on the top looking down

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29
Q

CN VI

A

Abducens (supplies the lateral rectus)

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30
Q

CN VII

A

Facial

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31
Q

CN VIII

A

Vestibulocochlear

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32
Q

IX

A

Glossopharyngeal

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33
Q

X

A

Vagus, efferent limb of the gag reflex,

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34
Q

XI

A

Acessory

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35
Q

XII

A

hypoglossal, in a lesion the tounge will deviate to the affected side

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36
Q

What is the next step in managment for a patient with new onset of Bell’s Palsy?

A

Steroids, if the symptomology is severe then consider acyclovir.

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37
Q

What is the most common complication of Bell’s palsy?

A

Corneal ulceration

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38
Q

If a patient has weakness first assess whether or not?

A

It’s true weakness then determine if the patient has UMN or LMN symptoms. If the patient has no sxm’s of the latter then consider another pathology like neuromuscluar junction issues, myopathy and electrolyte balance

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39
Q

Patient has presentation of being unable to move his right leg for the past 4 hours what area of the brain is compromised?

A

Left ACA

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40
Q

This stroke causes homonymous hemianopia without motor or sensory deficits

A

PCA

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41
Q

This stroke is purely motor/or purely sensory

A

Lacunar infarct

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42
Q

An ischemic stroke in the midbrain would affect what cranial nerves?

A

III and IV

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43
Q

An ischemic stroke in the pons would affect what cranial nerves

A

VI

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44
Q

An ischemic stroke at the medulla would affect what nerves

A

XII

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45
Q

A patient presents in the morning with onset of focal neurological deficit. He was noted to look normal prior to sleep the night before. CT is negative for hemorrhagic stroke, what is the next step in managment.

A

Because the timing for administration for TPA has passed (>4.5 hrs) we don’t give TPA instead we give an anti-platelet.

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46
Q

A patient presents with sudden onset of focal neurological deficit for the past 3 hours. CT is negative for hemorrhage what is the next best step in management?

A

Make sure that the blood pressure is controlled for <185/110. After the B/p is controlled we can start thrombolytics.

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47
Q

A patient that presents with focal neurological deficits has a positive CT scan for hemorrhage, what is the best next step in managment?

A

Stop anti-coagulation, if blood has entered the ventricles and there is evidence of hydrocephalus elevate, hyperventilate, and administer mannitol in the meantime thepatient should be prepped for surgical evacuation.

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48
Q

Antiplatelets like aspirin, clopidogrel should be started ____ hours after a CVA?

A

48 hours

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49
Q

What is the most common risk factor for a stroke?

A

HTN

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50
Q

What is the most common risk factor for a lacunar stroke?

A

HTN

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51
Q

Patients with hemorrahgic stroke tend to present with..

A

high ICP, bradycardia, abducens nerve palsy ( this is because most common area of a hemorrahic stroke is the MCA) and papilladema

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52
Q

What is the MCC of subarachnoid hemorrhage?

A

Berry aneurysm

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53
Q

A 60 yo M presents to the office with the worst headache he has ever had, and vomiting what is the dx?

A

Subarachnoid hemorrhage

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54
Q

If a CT scan is negative for hemorrhagic stroke, but your index of suspicion for a hemorraghic stroke is still high what is the best next step in mangament?

A

Lumbar puncture, only if the ICP is not too high. Xanthochromia

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55
Q

After you confirmed the diagnosis is hemorrhagic stroke what it the next step in managment?

A

Get an MRA to locate the aneurysm

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56
Q

What can we do to prevent vasospasm in a patient with a hemorrhagic stroke?

A

administer a calcium channel blocker to prevent vasospasm which is the most fatal side affect of a hemorrhagic stroke. The arteries of the brain constrict to prevent continued blood loss

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57
Q

A 70yo M with PMH of HTN, diabtetes, and CAD. Recently had a clipping procedure for a hemorrhagic stroke. Today post-op day 1 he complains of intense headache and nausea what intervention can reduce the ICP in this patient?

A

ventriculoperitoneal shunt

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58
Q

These signs and symptoms indicate peripheral veritgo.

A

spontaneous unidirectional horizontal nystagmus, absent skew deviation, and abnormal head impulse test (i.e., impaired vestibuloocular reflex).

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59
Q

A patient presents to the emergency room with the worst headache of his life what is the most likely dx?

A

Subarachnoid hemorrhage

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60
Q

What is the next step in management of a patient that has the worst headache of their life ?

A

A CT should be obtainied if that is inconclusive then we consider a lumbar puncture, xanthochromia would be suggestive of SAH.

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61
Q

What is the treatment for a patient with SAH?

A

Coiling or clipping

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62
Q

What are the complications of hemorrhage?

A

Vasospasm of the arteries causing infarction or ischemia. Hydrocephalus is also a complication that may require venrticuloperitoneal shunt

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63
Q

What is primary lateral sclerosis?

A

Selective involvement of the UMN

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64
Q

What is progressive muscular atrophy?

A

selective involvement of the LMN

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65
Q

Amyotrophic lateral sclerosis?

A

Involvement of both UMN and LMN does not have cognitive nor sensory affects.

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66
Q

What is the next step in management for diagnosing ALS ?

A

EMG (electromyographic studies) and nerve conduction studies.

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67
Q

What is MS?

A

It is an autoimmune attack on cells of the CNS resulting in demyelination.

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68
Q

What is the clinical presentation of MS?

A

optic neuritis, opthalmoplegia (inability to adduct the eye).

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69
Q

This phenomenon produces a shock like quality down the neck when the neck is flexed?

A

Lhermitte’s

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70
Q

What is the diagnostic testing for MS?

A

MRI with gadolinium contrast if that is not diagnostic then a lumbar puncture for IgG would be the next best step in management (it’s going to cytology.)

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71
Q

This disease presentation gets worse with repetitive movement.

A

Myasthenia gravis

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72
Q

What are the presentation of symptoms in a patient with myasthenia gravis?

A

Usually facial weakness (ptosis, facial droop), muscle weakness that gets worse throughout the day.

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73
Q

What is the diagnostic test for myasthenia gravis?

A

Edrophnium test followed by anti-bodies against ach receptors. If the anti-AChr is negative then we check for anti-musk antibodies (antimuscle specific tyrosine kinase antibody.

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74
Q

What are life threatening complications of myasthenic crisis or Gullian Barre?

A

Respiratory comprimise so we should monitor PFT

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75
Q

Ascending weakness, arreflexia, in a patient with a recent gastroenterits?

A

Gullian Barre

76
Q

What is the treatment for Gullian Barre?

A

IVIG and plasmapaharesis

77
Q

What is spondylotpathy?

A

Vertebral bone pathology

78
Q

What is spondylitic myelopathy?

A

vertebral bone or disc issues that lead to spinal cord dysfunction

79
Q

Myelitis?

A

Is spinal cord inflammation

80
Q

-spondylo think

A

bone

81
Q

-myelo think

A

spinal cord

82
Q

When should we consider an acute compressive myelopathy?

A

when the patient has fever, saddle anesthesia, urinary and fecal incontinence, hx of malignacny and trauma.

83
Q

What are causes of acute non-compressive myelopathies?

A

Spinal cord infarction and transverse myelitis

84
Q

What are the etiologies for transverse myelitis?

A

systemic diseases like SLE, sarcoidosis , infections (herpes is the most common), and demyelinating disorders like MS or acute transverse myelopathy.

85
Q

What is the next step in diagnosis of a patient you suspect to have a non-compressive myelopathy?

A

MRI of the spine with IV contrast if the MRI is negative for a compressive myelopathy we obtain a lumbar puncture.

86
Q

What is the next step in managment of a patient with a compressive myelopathy?

A

Administer steroids first and then the patient should undergo imaging followed by surgical intervention.

87
Q

Patient presents with loss of sensation of pain and temperature and bilateral weakness.

A

This anterior cord syndrome. It is the most common spinal cord infarction with the spinal artery.

88
Q

Patients with a spinal infarct have an acute or chronic presentation?

A

Acute

89
Q

Spinal cord infarcts will mainly present bilaterally or unilaterally?

A

bilaterally

90
Q

Patient present with loss of orientation in space and cannot feel any sensation in his lower limbs what is the diagnosis?

A

Posterior cord syndrome

91
Q

A patient who was stabbed in the back presents to the ED with complete paralysis on the right side with loss of vibration on the same side and loss of pain in temperature in his left leg. What is the diagnosis?

A

Brown Sequard

92
Q

What is syringomyelia?

A

It is cystic formation in the spinal cord it is also the MCC of central cord syndromes.

93
Q

This patient has weakness and loss of temperature and pain sensation in a shawl like distribution

A

Central cord syndrome

94
Q

What are some of the causes of spondylomyelopathies?

A

Narrowing of the space due to disc degeneration, bone spur formation, sclerotic facet joint.

95
Q

What symptoms would we see in a patient spondylotic myelopathy?

A

Radicular pain, muscle weakness,

96
Q

POUND is a pneumonic to remind yo u of the symptomology seen in migrane headaches

A

Pwulsating, one day duration, unilateral location, nausea, disabling

97
Q

What is Aura?

A

Characteristic sensory symptoms before the onset of headache

98
Q

what are prophylactic treatments for migranes?

A

Beta blockers, antidepressants or anti-convulsants

99
Q

True or False OCP’s are contraindicated in patients with migranes?

A

True

100
Q

A patient with headache, ptosis of the right eye, tearing of the right eye, the patient says that he has been experiencing these headaches for months that come and go. What is the next step in treatment?

A

100% oxygen and a triptan, verapamil is a prophylactic drug

101
Q

band like headache that tends to progress with stress?

A

Tension headache

102
Q

What is the treatment for trigeminal neuralgia

A

First line is carbamazipine, second line gababpentine, third line surgery to remove compression

103
Q

A patient comes to to office with complaints of dizziness what are the two types of dizziness a patient could be reffering to?

A

Vertigo (the room is spinning) or presyncope

104
Q

What are signs of peripheral vertigo?

A

Tinnitus or hearing loss

105
Q

What are the cause of peripheral vertigo?

A

Menieres disease, vestibular neuronitis vestibular labrynthitis, BPPV, perilympahatic fistula, vestibular schwannoma, motion sickness

106
Q

Intermittent vertigo + hearing loss + tinnitus =

A

Meniere’s disease which is due to increased endolymph production

107
Q

What is the next step in management for Meniere’s disease?

A

Rule out syphilis by VDRL or RPR, encourage salt restriction and diuretices

108
Q

Sudden acute onset of vertigo lasting for several days with no tinnitus or hearing loss?

A

Vestibular neuronitis

109
Q

Suddnen onset of vertigo with hearing loss and tinnitus that has never happened before

A

Vestibular labrynthitis

110
Q

Transient vertigo that is exacerbated by head movement.

A

BBPV

111
Q

What is the diagnostic study for BBPV ?

A

Dix hallpike

112
Q

What is the treatment for BPPV?

A

Epley’s manuver

113
Q

Progressive symptoms of non-specific vertigo and asymmetric hearing loss.

A

Vestibular schwannoma

114
Q

Vertigo associated with motion?

A

Motion sickness

115
Q

What constitutes orthostatic/postural syncope?

A

when blood pressure drops from lying down to standing to >20 in systolice and >10 in diastolic.

116
Q

What is the cause of vasovagal?

A

Parasympathetic overdrive

117
Q

What is the diagnostic test for vasovagal?

A

Tilt table test

118
Q

How do we differentiate a seizure from syncope?

A

Aura, Confusion, Amnesia, Tounge biting, continenece, and headache. “ A CATCH”

119
Q

What are causes for seizures?

A

VITAMINS, vascular, infection, trauma, autoinmmune, alcohol, metabolic, idiopathic, neoplastic, and psychiatric.

120
Q

Of the two types of seizure general and partial. What are the types of partial seizures?

A

Simple (patient is concious and can respond to external stimuli) and complex (patient maintains conciousness, but cannot respond to external stimuli

121
Q

What can happen to the anion gap in a patient experiencing seizures.

A

Tonic Clonic (spastic muscles that contract, atonic (where there is a brief loss of muscle tone), absence seizure and myoclonic which are brief muscle contractions

122
Q

What may be elevated in the BNP after a seizure?

A

elevated lactate

123
Q

A patient with absence seizure would show _____ on EEG

A

3hz spike and wave discharge

124
Q

What is the treatment for absence seizures?

A

ethosuxamide

125
Q

What is the diagnostic process for a patient that has experienced and absence seizure

A

Obtain electrolytes and CT scan without contrast, then get and EEG and MRI

126
Q

When a patient is seizing for > 5mins we call this?

A

Status epilecticus

127
Q

What is the most common cause of status epileticus

A

persons with low antiepilectic medication level

128
Q

What is the first line drug for a partial seizure?

A

Carbmazapine

129
Q

When is it safe to discontinue an anti-epiletic drug?

A

If a patient after two years has no experienced headaches we do a sleep deprivation test if that does not illicit seizure

130
Q

What are the side affects of phenytoin?

A

Hepatic failure, gingival hyperplasia and SJS

131
Q

What are the side affects of carbamazipine?

A

Teratogen can cause, SJS hepatic failure

132
Q

What should we do for drug treatment of a patient that is pregnant with seizure disorder?

A

use the lowest dosage of AED

133
Q

Patients that are planning to become pregnant with seizure disorder should take what seizure medication?

A

valproate

134
Q

What is dementia?

A

memory loss +the impairment of being able to do daily activities

135
Q

Dementia + urinary incotinence + broad based gate =

A

normal pressure hydrocephalus

136
Q

Dementia with fluctuating course + visual hallucination

A

Lewy body dementia

137
Q

Dementia + Age of patient is <50, writhing movements (slow involuntary movemets) ,

A

Huntingtons

138
Q

Dementia + EEG abnormalities and sudden jerky movements

A

Spongiform encephalopathy

139
Q

Personality change + dementia

A

Frontotemporal dementia

140
Q

Dementia that gets progressively worse in an athersclerotic patient

A

vascular dementia

141
Q

Normal pressure hydrocephalus occurs due to?

A

CSF absorption

142
Q

(True or False) Patients with normal pressure hydrocephalus have normal pressure values on vertebral tap?

A

True, but the patients will also have releif with draingage of CSF

143
Q

What area of the brain does Huntington’s disease manifest?

A

Caudate and you can remember this by chorea = caudate

144
Q

This is a neurodegenerative disorder of alpha-synnuclein in the brain

A

Lewy

145
Q

This is a neurodegenerative disorder of abnormal tau protien deposit

A

frontotemporal dermentia

146
Q

This is a neurodegenerative disorder of amyloid protein

A

Alzhimers

147
Q

What is the symptomology for parkinsons?

A

BRITS have parkinsons, Bradykinesia, rigidity, instable posture, tremor, and shuffling gate. ( The patient must present with bradykinesia + one other RITS presentation in order to be diagnosed

148
Q

Drug of choice for Alzhemimers

A

Acetocholinesterase (donepizil)

149
Q

Drug of choice for Parkinsons?

A

anticholinergic drugs (specifically for relief with tremors)

150
Q

A tremor that worsens with goal directed activity and alcohol typically resolves the symptoms.

A

Essential tremor

151
Q

What is the treatment for an essential tremor

A

propanolol and primidone

152
Q

Tremor worsens with activity, but is also associated with ataxia or nystagmus

A

intention tremor

153
Q

Tremor at rest

A

parkinsons

154
Q

What is the treatment for an intention tremor.

A

beta blocker

155
Q

What are some of the cause for carpal tunnel?

A

Overuse, hypothyroidism, pregnancy DM and amyloidosis.

156
Q

What is the next step in diagnosing carpal tunnel?

A

EMG and nerve conduction

157
Q

What is the treatment for carpal tunnel?

A

splint first, then steroids, then surgery to cut the flexor retinaculum

158
Q

Paraesthesia in the medial foot when compression on the back of the leg?

A

Tarsal tunnel

159
Q

What is treatment for a patient with tarsal tunnel?

A

orthotics , steroids, surgery

160
Q

Paraesthesia in the lateral abdomen and thigh especially when wearing tight pants.

A

Meralgia paresthertica

161
Q

Multiple peripheral nerves involvement?

A

mononeuritis multiplex

162
Q

Symmetric distal to proximal parathesias (glove stocking distribution)

A

Axonal polyneuropathies

163
Q

The most common benign intracranial tumor, appears calcified on histology.

A

Meningioma

164
Q

True/False a solitary metastasis to the brain should be resected?

A

True, if this is mets to the brain with multiple lesions then we do radiation, but if it’s one nodule then resect.

165
Q

What are the drugs of choice when treating restless leg syndrome?

A

Pramipexole, ropinorole

166
Q

Brain death =

A

no cranial nerve reflexes and no spontaneous respirations

167
Q

What are the symptoms of Acute intermittent porphyria (AIP)

A

Pain, Peripubertal onset, phenobarbital, psychosis, peripheral neuropathy.

168
Q

What is the diagnostic test for AIP?

A

porphyrins rings in the urine and increased levels of porphobilinogen

169
Q

What are the characteristics of a low risk headache?

A

No change in the type of headache, no focal neurological deficits, no thunderclap, some patient may have aura that results in transient vision loss

170
Q

What are the characteristics of a high risk headache?

A

Worst headache of my life, focal neurological deficits, worse with sneezing coughing, and neck stiffness

171
Q

What criteria must a patient meet in order to diagnose a cluster headache?

A

The patient has pain in the eye and should display tearing, reddening, sweating, ptosis.

172
Q

_____ should be done prior to doing a lumbar puncture to prevent brain herniation.

A

CT scan

173
Q

Close contacts of patients with Nisseria Meningitis should recieve what prophylaxis?

A

cefrtriaxone, ciprofloxaicn, or rifampin

174
Q

Infants before the age of 6 months with muscle weakness, what is the diagnosis?

A

Spinal muscular atrophy or Werdnig Hoffman

175
Q

Patient presents with muscular weakness that gets worse throughout the day. The patient has facial droop, ptosis, diplopia, and dysphagia what is the likely diagnosis?

A

Myasthenia gravis

176
Q

Normal deep tendon reflexes in a patient with muscular weakness suggest?

A

a myopathy as opposed to nerve pathology.

177
Q

Patient presents with sudden, painless visual loss. In this case, the patient was experiencing intermittent loss of vision (known as amaurosis fugax). Patients may also have antecedent or simultaneous headache, jaw claudication, tenderness over superficial temporal arteries, proximal muscle and joint aches, anorexia and weight loss. what is the diagnosis?

A

Giant cell arteritis

178
Q

Patients with Herpes Simplex meninigitis will have what unique finding on CSF

A

RBC’s

179
Q

What is the MC organims of viral meningitis?

A

Enteroviruses (poliovirus, cocksakie A and B, rhinovirus)

180
Q

What are the most common causes of viral meningitis in children <1 month?

A

BEL (Group B strep, Ecoli, and Listeria)

181
Q

What is the most common cause of viral encephalitis?

A

HSV

182
Q

What are some differences between the presentation of meningitis and encephalitis?

A

If we suspect encephalitis patients typically present with a prodrome of headaches and fever, followed by sudden focal neurological deficits, seizures, and altered mental status. Meningitis presents with photophobia, neck rigidity, AMS, and headache + brudzinski

183
Q

What is the MC cause of bacterial meningitis in adults?

A

Strep pneumoniae

184
Q

What is the pathology behind normal pressure hydrocephalus?

A

lack of CSF reabsorption (idiopathic or due to lack of reabsorption by the subarachnoid villi).

185
Q

Increased CSF production (due to choroid plexus neoplasia or inflammation) causing enlarged ventricles, it typically manifests with signs of intracranial hypertension (e.g, headache, nausea, vomiting) rather than the symptoms seen in this patient, what is the diagnosis?

A

Communicating hydrocephalus

186
Q

This patient because of obstructed flow of the CSF presents with increases ICP, headaches, papillidema etc.

A

Non-communicating hydrocephalus

187
Q

What is Cushing’s triad

A

Bradycardia, high blood pressure. This occurs to maintain perfusion to the brain increasing arterial smooth muscle vasoconstriction. This initiates the parasympathetic response causing bradycardia.

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