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Clinical Medicine III > Exam II > Flashcards

Exam II Flashcards

1
Q

Ischemic stroke

A

Thrombotic or embolic occlusion of an artery stopping blood flow to a cerebral area

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2
Q

Hemorrhagic stroke

A

Bleeding from an blood vessel due to leakage/rupture

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3
Q

TIA (transient ischemic attack)

A

Temporary occlusion of cerebral vessel which gets resolved within 24 hours, warning sign of stroke coming in near future)

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4
Q

Early warning signs of stroke

A

BE FAST

Balance difficulties, eyesight changes, face weakness, arm weakness, speech difficulties, time (call 911)

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5
Q

ABCD prediction scale (chances of TIA progressing to stroke)

A

Age > 60
BP: >140/>90
Clinical Presentation:
-Unilateral weakness
-speech impairment without weakness
Diabetes
Duration of TIA
->60 minutes, 10-59 minutes

Risk of stroke at 2 days

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6
Q

Ischemic stroke pathogenesis

A

Occlusion of major arteries
-either directly by thrombus formation
-or by embolus

Vascular causes:
-Atherosclerosis
-Artery-to-artery embolism

Cardiogenic causes
-A-fib
-MI
-Valve diseases

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7
Q

CBF impairments following Ischemia

A

Normal average CBF is 50 ml/100 g/min

Average cerebral perfusion pressure (CPP) is about 60mmHg

If CBF falls below 20 mL/100 g/min, neuronal functioning is impaired. If it falls below 8-10 mL/100 g/min, tissue death occurs

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8
Q

Middle cerebral artery distribution

A

Biggest distribution - supplies dorso-lateral regions of frontal/parietal lobes, temporal lobe, basal ganglia nuclei and internal capsule

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9
Q

Anterior cerebral artery distribution

A

Supplies medial regions of frontal and parietal lobes and anterior region of frontal lobe

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10
Q

Posterior cerebral artery distribution

A

Supplies all occipital lobe, inferior regions of temporal lobe (hippocampus), midbrain (cerebral peduncles) and thalamus

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11
Q

Vertebrobasilar system

A

(from 2 vertebral arteries providing collateral circulation) – supplies brainstem and cerebellum

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12
Q

SCA (superior cerebellar artery) distribution

A

cerebellar cortex, cerebellar nuclei, superior cerebellar peduncle, and a small portion of midbrain

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13
Q

AICA (anterior inferior communicating artery) distribution

A

supplies CN nuclei V/VII/VIII, vestibular and hearing organs (via labyrinthine artery) – helps with differential diagnosis

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14
Q

PICA (posterior inferior communicating artery) distribution

A

arises from vertebral arteries, supplies dorsolateral medulla, posterior portion of the cerebellar hemispheres and the central nuclei of the cerebellum, CN nuclei V/IX/X

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15
Q

Prefrontal functional area

A

ACA & MCA

Judgement, foresight, problem solving, behavior, social appropriateness

Lesion – poor judgement, apathy, poor motivation, flat affect, social inappropriateness, perseveration

Due to connections between Dorsolateral Prefrontal cortex to Basal Ganglia - may have difficulty with dual tasking and motor planning.

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16
Q

Premotor functional area

A

MCA

Motor planning area (externally guided movements) – reaching, grasping

Lesion – ideomotor apraxia (motor planning problem) – inability to perform a task in response to a verbal command or imitate gestures.
Patient knows what they want to do but cannot plan the motor plan needed to complete a task

problems with bimanual tasks

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17
Q

Supplementary Motor functional area

A

ACA

Motor planning area (internally guided movements)
Lesion – ideomotor apraxia

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18
Q

Primary Motor functional area

A

ACA & MCA

Execution of voluntary skilled movements on opposite side

lateral cortex – UE, upper trunk and face

medial cortex – LE, lower trunk

Lesion – lack of voluntary skilled movement

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19
Q

Primary Sensory functional area

A

ACA & MCA

Detection and localization of sensation from the opposite side of the body and face

lateral cortex – UE, upper trunk and face

medial cortex – LE, lower trunk
Lesion – loss of sensation

impaired balance

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20
Q

Sensory Association functional area

A

Sensory processing and sensory perception (making sense of the senses)

Lesion (in parietal lobe areas)

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21
Q

ideational apraxia

A

failure to perceive/conceptualize a sensory environment due to impaired cross-modal processing, so unable to understand the purpose of tools/objects because of loss of higher-level perception (use a toothbrush to comb one’s hair)

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22
Q

Frontal Eye Fields functional area

A

MCA

Controls voluntary saccadic eye movements and smooth pursuits

Lesion – eyes deviate towards the lesion (look away from paralysis)

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23
Q

Wernicke’s area

A

MCA and PCA (dominant hemisphere – usually left)

Language comprehension

Lesion – patient cannot comprehend speech. Patient can speak fluently, but output makes no sense, fluent/receptive aphasia

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24
Q

Broca’s area

A

MCA (dominant hemisphere – usually left)

Expressive language (speak, write, sign etc.)

Lesion – inability to express one’s self through language (but comprehension is intact), nonfluent/expressive aphasia

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25
Q

Primary Visual functional area

A

PCA

Perceives visual information coming from the retina

Lesion – cortical blindness, loss of vision in contralateral ½ of the visual field, but patient may not feel the loss (visual agnosia)

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26
Q

Visual Association area

A

PCA

Makes sense of vision – recognizes faces, objects

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27
Q

Internal Capsule functional area

A

MCA (Lenticulostriate arteries)

Sensory
contralateral loss of pain, temperature, touch and proprioception from entire extremities and face

Motor
contralateral weakness of all muscles of the body

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28
Q

Midbrain functional area

A

Basillar artery, PCA, SCA

Sensory
Spinal Lemniscus (Pain and temp), Medial Lemnicus (touch and proprio)

Motor
Cranial nerve nuclei III, IV, MLF (causes internuclear ophthalmoplegia), corticobulbar tract, corticospinal tract

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29
Q

MCA syndrome (63% of ischemic strokes)

A

Clinical presentation:
-Contralateral weakness (UE and face)
-Contralateral sensory impairment (UE and face)
-Aphasia (L/dominant hemisphere) – expressive, receptive, global
-Neglect (R/nondominant hemisphere)

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30
Q

ACA Syndrome (6-7% of ischemic strokes)

A

Clinical presentation:
Sensory impairment in contralateral LE
Weakness in contralateral LE
Altered mental status
aphasia
Abulia (a lack of drive/will power)

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31
Q

Posterior Cerebral Artery Syndrome (12-13% of ischemic strokes)

A

-Contralateral homonymous hemianopsia
-Contralateral limb weakness
-Thalamic pain syndrome (abnormal sensations of temperature/proprioception/touch, tingling, paresthesia, intractable pain, allodynia)
Visual agnosia, anomia

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32
Q

Lacunar Syndrome (5-8%)

A

-Small infarcts at the end of deep penetrating arteries, often affecting white matter. Areas affected are basal ganglia, internal capsule, brainstem, and thalamus.

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33
Q

Lacunar Syndrome clinical manifestations

A

Clinical Presentation (depends on area affected):
-Pure contralateral weakness (posterior limb of internal capsule)
-Pure contralateral sensory loss (posterolateral thalamus or posterior limb of internal capsule)
-Parkinsonism (basal ganglia)

large majority are asymptomatic

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34
Q

VertebroBasilar Artery Syndrome clinical manifestations

A

Headache, D/N/V, diplopia, nystagmus, dysarthria, dysphagia

ipsilateral ataxia, dysmetria, and hemiparesis

Bilateral effects if trunk of basilar artery is occluded.

Locked in syndrome due to stroke in basilar artery

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35
Q

Superior Cerebellar Artery Syndrome clinical presentation

A

Headache, D/N/V, Nystagmus, diplopia, dysarthria, ipsilateral ataxia, ipsilateral horners syndrome

Contralateral loss of touch/pain/temp in extremities, torso, and face, if any

Contralateral mild hemiparesis, if any

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36
Q

Anterior Inferior Cerebellar Artery Syndrome (AICA/lateral pontine syndrome) clinical manifestations

A

-D/N/V, nystagmus, diplopia, dysarthria, dysmetria
-Ipsilateral deafness
-ipsilateral ataxia
-ipsilateral horners syndrome

Ipsilateral loss of touch/pain/temp and weakness in face

Contralateral loss of pain/temp and weakness in limbs, if any

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37
Q

Posterior Inferior Cerebellar Artery (PICA) clinical manifestations

A

Results in Lateral medullary syndrome or Wallenberg Syndrome

D/N/V, nystagmus, dysarthria, ipsilateral ataxia, ipsilateral horners syndrome, dysphagia, hoarseness of voice

Ipsilateral loss of touch/pain/temp on face (CN V nucleus)

Contralateral loss of pain/temp on body, if any

38
Q

Spinal artery and vertebral arteries

A

Results in Medial medullary syndrome

Supplies: medial medulla

Clinical presentation:
-contralateral paresis of U&LE
-Contralateral loss of touch and proprioception
-Ipsilateral tongue deviation (hypoglossal nucleus)

39
Q

NIH stroke scale

A

Not used for diagnosing nature or location of stroke, but to assess severity of stroke

0 - no stroke
0-4 - minor stroke
5-15 - moderate stroke
16-20 - moderate to severe stroke
21-42 - severe stroke

≥ 16 forecasts a high probability of death or severe debility
≤ 6 forecasts good recovery

40
Q

MRI/PET imaging for stroke

A

Helps with localizing stroke – lobe, structures that are damaged

Severity/area of damage

Detects the area of ischemic penumbra

Determine who would be ‘good candidate’ for continued use of thrombolytic drugs

41
Q

Hemorrhagic stroke

A

Bleeding from an arterial source

Types
Intracerebral hemorrhage
Subarachnoid Hemorrhage
Subdural Hemorrhage
Epidural Hematoma

42
Q

Intracerebral hemorrhage (ICH)

A

Bleeding into brain parenchyma, most deadly, Incidence low among young people, increases dramatically after 65 years of age

Risk factors – chronic HTN, alcohol abuse, substance abuse, chronic thrombolytic therapy, smoking, eclampsia during pregnancy

43
Q

pathogenesis of ICH

A

Dysfunction in cerebral microvasculature secondary to chronic HTN. Weakening of arterial walls and more prone to aneurysms rupture/leakage.

Mostly in smaller deep penetrating arteries - lenticulostriates, arteries entering thalamus, brainstem

44
Q

Clinical manifestations of ICH

A

Similar types of clinical presentation as ischemic stroke

Initial symptoms are related to area where bleed occurs

Additional neurologic symptoms occur gradually representing expansion of hematoma

As bleed enlarges ICP may increase causing headache, vomiting and decreased alertness.

Seizures

45
Q

Subarachnoid hemorrhage (SAH)

A

Bleeding into subarachnoid space
Another deadly type – mortality 40-60%

Mostly in older (>70 yr) women
Risk factors – HTN, alcohol abuse, smoking

46
Q

Etiology of SAH

A

Berry aneurysms – abnormal local distension occurring at vessel bifurcations

About 90% of SAH are due to berry aneurysms

47
Q

Clinical manifestations of SAH

A

Sudden onset with severe ‘thunderclap’ headache – sudden and severe

Sentinel headache/Sentinel bleeds – warn sign of SAH - preceding aneurysm ruptures by days or weeks

At the time of rupture, additional symptoms include N/V, altered mental status (syncope, confusion, coma), lethargy, seizure, neck pain, nuchal rigidity

Focal neurological signs like hemiplegia or hemianopia are absent, unless bleeding into brain parenchyma

48
Q

Medical management of SAH

A

Treatment
Immediate neurosurgery to isolate the aneurysm or rupture site, evacuate hematoma to prevent further damage

Prognosis
Mortality is high in elderly
If hematoma is <3cm, prognosis is good

49
Q

Subdural hemorrhage

A

Result of tearing of bridging veins, mostly occur in elderly after falls, If blood accumulates, compression of brain tissue, can result in herniation of cortex into adjoining spaces

50
Q

Epidural hemorrhage

A

Result of tearing of meningeal arteries that run in between the dura

Can be torn secondary to trauma

Medical emergency, need immediate evacuation to prevent compression of brainstem structures, which may cause death.

51
Q

Mild TBI

A

majority kind, also called concussions, symptoms generally self-limiting and temporary, less severe end of TBI, but still can involve complex pathophysiology

52
Q

Moderate to severe TBI

A

Loss of consciousness from several minutes to hours, persistent headache, vomiting or nausea, convulsions or seizures

53
Q

Open TBI

A

Penetrating lesions – fractures, gunshots (velocity and not the size of projectile often determine extent of damage)

Meninges are breached

Can cause damage to brain parenchyma, vascular damage (formation/disruption of aneurysms)

54
Q

Closed TBI

A

No skull fracture or penetrating injury, but brain experiences forceful contact on the inner side of hard bony skull, can occur without head hitting hard surface (whiplash), can cause diffuse injuries. Symptoms worse if there is rotational component

Can lead to coup-contre-coup type injuries

55
Q

Increased Intracranial pressure (ICP)

A

Most critical secondary injury mechanism, needs to be monitored and controlled, can be due from mass effects from hematoma, cerebral edema, hydrocephalus, increased CBF due to other metabolic reasons, CSF outflow blockage

56
Q

Consequences of increased ICP are…

A

triggers a vicious cycle vascular dysregulation,

Normally, brain can maintain constant average CBF by automatically regulating CPP (cerebral perfusion pressure) over a range of mean arterial pressure, MAP (50-150mmHg), using cerebral auto-regulatory mechanisms.

CPP = MAP - ICP, auto regulation is disrupted

57
Q

Postraumatic aneurysms

A

Delayed vascular change, due to weakening of cerebral arteries overs days to years (average 3 weeks). can develop in internal carotid artery inside the cavernous sinus. Due to proximity of internal carotid artery to CNs II, III, IV, V, VI.

58
Q

Vasogenic edema

A

due to fluid leaking from disrupted BBB along endothelial linings

59
Q

Cytotoxic edema

A

due to disruption of NA/K ion pumps leading to water entry and retention

60
Q

Osmotic edema

A

due to osmolar property changes between extra and intra cellular fluids, causing water entry.

61
Q

Compressive damage

A

Increased ICP due to mass bleeding and edema can compress brain tissue. Compression causes midline shift, brain tissue tries to push into openings or spaces, as herniations.

62
Q

Transtentorial herniation of uncus

A

shifts the brainstem, pushes against the contralateral tentorium

63
Q

Headache

A

Most common complaint after TBI, Migraine headaches w/ w/o may develop hours or weeks after

In moderate and severe TBI, if headache appears later and person deteriorates neurologically after being lucid initially after injury, then suspect increased ICP from hematoma, need to monitor and treat urgently

64
Q

Concussion (mild TBI) clincial manifestations

A

Short-lived impairment of neurologic functions that resolve spontaneously, typically within 7-10 days

Headache, dizziness, nausea, cognitive problems, fatigue and sleep disturbances/sleeping more than usual.

Factors that may prolong recovery time are LOC for >1minute, significant cognitive problems, younger age, female gender and depression

65
Q

Signs at different levels of Consciousness/disorders of consciousness

A

Coma is lowest level of consciousness, rarely lasts for more than 4 weeks

wakeful post-comatose unawareness (PVS)

Minimal conscious state (can track objects visually, inconsistent ability to follow commands, simple communications (yes/no gestures))

66
Q

Decorticate posturing/rigidity clinical manifestations

A

sustained posturing of UE in flexion and LE in extension

If situation continue to worsen, Decerebrate posturing/rigidity – sustained posturing of UE/LE and trunk on full extension

Compression of brainstem vital centers can elicit abnormal pulse rate, respiratory rate, BP changes, excessive sweating, salivation.

67
Q

Decorticate posturing

A

due to compression of cortical connections to the red nucleus, resulting in disinhibited rubrospinal activity

68
Q

Decerebrate posturing

A

due to further compression cortical connections to reticular/vestibular nuclei, resulting in disinhibited reticulospinal/vestibulospinal activity

69
Q

Cheyne-Stokes breathing

A

rhythmic pattern of increasing/decreasing rate of breathing, bilateral hemispheric or midbrain lesions

70
Q

Hyperventilation

A

‘overbreathing’ where blood CO2 decreases causing respiratory alkalosis – pontine/midbrain lesions

71
Q

Apneustic breathing

A

prolonged pause at the end of inspiration – mid- to lower pons lesions

72
Q

Ataxic breathing

A

irregular rate and depth of breathing – medullary lesions

73
Q

Motor deficits associated with TBI

A

Hemispheric lesions can involve one limb or cause hemiplegia, cerebellar lesions can cause ataxia, basal ganglia lesion can cause tremors/bradykinesia.

Flaccidity can gradually be replaced by spasticity

Movement disorders can occur immediately due to acute trauma, or can develop later (dystonia)

74
Q

Kernohan’s notch phenomenon

A

due to transtentorial herniation,

If cerebral peduncles are compressed against contralateral tentorium - false localizing signs, resulting in ipsilateral hemiplegia

75
Q

CN damage due to TBI

A

Eye exam can yield valuable info about coma – if completely normal pupillary reaction – suggests lesion is above midbrain

CN II damage in optic canal (most vulnerable area of the nerve) –monocular blindness, and bilateral loss of pupillary reaction

76
Q

Pain associated with TBI

A

Headache and neck pain common with whiplash, Neuropathic pain, thalamic pain (allodynia), painful leg and moving toes syndrome, fibromyalgia

77
Q

Heterotopic Ossification

A

Abnormal bone growth in periarticular soft tissue (muscles/tendons)

Can be associated with trauma, immobility or spasticity following injury

Onset about 4-12 weeks after injury

First detected as tenderness, swelling, pain with movements, loss of ROM, later can be palpated as mass

78
Q

Second Impact Syndrome (with successive concussions)

A

Effect of a second concussion before the brain has a chance to recover fully results in worse clinical presentation, Second injury can cause rapid/severe disruption of cerebral autoregulation, LOC and progressive disability or death if not monitored and treated.

79
Q

Chronic traumatic encephalopathy (CTE)

A

Progressive degenerative condition, thought to be caused by multiple repeated concussive blows over a lifetime. Deterioration in cognition and behavior.

evidence of degeneration, deposition of protein Tau

80
Q

Moderate/Severe TBI in ICU/Acute settings medical management

A

Goals - Assess LOC, assess severity, changes in severity, locate lesion

Pupillary response and oculomotor signs - valuable in diagnosis depth of LOC and localizing brainstem damage

Sluggish or unreactive pupillary response may indicate severe TBI, or increased severity with increasing ICP with successive exams

Gaze palsies – lesion of oculomotor nerves on one side, tonic downward gaze – compression of thalamus, ocular bobbing – pontine lesion

81
Q

Mild TBI (Concussion) treatment

A

most recover fully in 7-10 days, Concussed brain is less responsive to usual neural activation, and if premature cognitive and physical activity is forced before complete recovery, it can be vulnerable to prolonged dysfunction. So need to rest – including cognitive rest, avoid repeat concussion

82
Q

Coma sign when associated with herniation

A

compression of the midbrain tegmentum, uncal and central herniation

83
Q

Pupillary dilation associated with herniation

A

Compression of ipsilateral third nerve, uncal herniation

84
Q

Miosis associated with herniation

A

compression of the midbrain, Central herniation

85
Q

lateral gaze palsy associated with herniation

A

stretching of the 6th nerve, central herniation

86
Q

Hemiparesis associated with herniation

A

compression of contralateral cerebral peduncle against tentorium, uncal herniation. May occur ipsilateral to hemispheric lesion due to false localizing

87
Q

Decerebrate posturing associated with herniation

A

compression of the midbrain, central and uncal herniation

88
Q

Hypertension. bradycardia associated with herniation

A

compression of the medulla, central, uncal, and cerebellar (tonsillar)

89
Q

Abnormal breathing patterns associated with herniation

A

compression of the pons and medulla. Central, uncal, and cerebellar (tonsillar)

90
Q

Posterior cerebral artery infarction associated with herniation

A

vascular compression, uncal herniation

91
Q

Anterior cerebral artery infarction associated with herniation

A

vascular compression, Subfalcine (cingulate)

Clinical Medicine III (4 decks)

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