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Clinical Medicine III > Exam II > Flashcards

Exam II Flashcards

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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
Primary Visual functional area
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)
26
Visual Association area
PCA Makes sense of vision – recognizes faces, objects
27
Internal Capsule functional area
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
28
Midbrain functional area
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
29
MCA syndrome (63% of ischemic strokes)
Clinical presentation: -Contralateral weakness (UE and face) -Contralateral sensory impairment (UE and face) -Aphasia (L/dominant hemisphere) – expressive, receptive, global -Neglect (R/nondominant hemisphere)
30
ACA Syndrome (6-7% of ischemic strokes)
Clinical presentation: Sensory impairment in contralateral LE Weakness in contralateral LE Altered mental status aphasia Abulia (a lack of drive/will power)
31
Posterior Cerebral Artery Syndrome (12-13% of ischemic strokes)
-Contralateral homonymous hemianopsia -Contralateral limb weakness -Thalamic pain syndrome (abnormal sensations of temperature/proprioception/touch, tingling, paresthesia, intractable pain, allodynia) Visual agnosia, anomia
32
Lacunar Syndrome (5-8%)
-Small infarcts at the end of deep penetrating arteries, often affecting white matter. Areas affected are basal ganglia, internal capsule, brainstem, and thalamus.
33
Lacunar Syndrome clinical manifestations
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
34
VertebroBasilar Artery Syndrome clinical manifestations
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
35
Superior Cerebellar Artery Syndrome clinical presentation
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
36
Anterior Inferior Cerebellar Artery Syndrome (AICA/lateral pontine syndrome) clinical manifestations
-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
37
Posterior Inferior Cerebellar Artery (PICA) clinical manifestations
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
Spinal artery and vertebral arteries
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
NIH stroke scale
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
MRI/PET imaging for stroke
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
Hemorrhagic stroke
Bleeding from an arterial source Types Intracerebral hemorrhage Subarachnoid Hemorrhage Subdural Hemorrhage Epidural Hematoma
42
Intracerebral hemorrhage (ICH)
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
pathogenesis of ICH
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
Clinical manifestations of ICH
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
Subarachnoid hemorrhage (SAH)
Bleeding into subarachnoid space Another deadly type – mortality 40-60% Mostly in older (>70 yr) women Risk factors – HTN, alcohol abuse, smoking
46
Etiology of SAH
Berry aneurysms – abnormal local distension occurring at vessel bifurcations About 90% of SAH are due to berry aneurysms
47
Clinical manifestations of SAH
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
Medical management of SAH
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
Subdural hemorrhage
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
Epidural hemorrhage
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
Mild TBI
majority kind, also called concussions, symptoms generally self-limiting and temporary, less severe end of TBI, but still can involve complex pathophysiology
52
Moderate to severe TBI
Loss of consciousness from several minutes to hours, persistent headache, vomiting or nausea, convulsions or seizures
53
Open TBI
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
Closed TBI
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
Increased Intracranial pressure (ICP)
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
Consequences of increased ICP are...
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
Postraumatic aneurysms
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
Vasogenic edema
due to fluid leaking from disrupted BBB along endothelial linings
59
Cytotoxic edema
due to disruption of NA/K ion pumps leading to water entry and retention
60
Osmotic edema
due to osmolar property changes between extra and intra cellular fluids, causing water entry.
61
Compressive damage
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
Transtentorial herniation of uncus
shifts the brainstem, pushes against the contralateral tentorium
63
Headache
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
Concussion (mild TBI) clincial manifestations
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
Signs at different levels of Consciousness/disorders of consciousness
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
Decorticate posturing/rigidity clinical manifestations
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
Decorticate posturing
due to compression of cortical connections to the red nucleus, resulting in disinhibited rubrospinal activity
68
Decerebrate posturing
due to further compression cortical connections to reticular/vestibular nuclei, resulting in disinhibited reticulospinal/vestibulospinal activity
69
Cheyne-Stokes breathing
rhythmic pattern of increasing/decreasing rate of breathing, bilateral hemispheric or midbrain lesions
70
Hyperventilation
‘overbreathing’ where blood CO2 decreases causing respiratory alkalosis – pontine/midbrain lesions
71
Apneustic breathing
prolonged pause at the end of inspiration – mid- to lower pons lesions
72
Ataxic breathing
irregular rate and depth of breathing – medullary lesions
73
Motor deficits associated with TBI
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
Kernohan’s notch phenomenon
due to transtentorial herniation, If cerebral peduncles are compressed against contralateral tentorium - false localizing signs, resulting in ipsilateral hemiplegia
75
CN damage due to TBI
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
Pain associated with TBI
Headache and neck pain common with whiplash, Neuropathic pain, thalamic pain (allodynia), painful leg and moving toes syndrome, fibromyalgia
77
Heterotopic Ossification
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
Second Impact Syndrome (with successive concussions)
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
Chronic traumatic encephalopathy (CTE)
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
Moderate/Severe TBI in ICU/Acute settings medical management
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
Mild TBI (Concussion) treatment
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
Coma sign when associated with herniation
compression of the midbrain tegmentum, uncal and central herniation
83
Pupillary dilation associated with herniation
Compression of ipsilateral third nerve, uncal herniation
84
Miosis associated with herniation
compression of the midbrain, Central herniation
85
lateral gaze palsy associated with herniation
stretching of the 6th nerve, central herniation
86
Hemiparesis associated with herniation
compression of contralateral cerebral peduncle against tentorium, uncal herniation. May occur ipsilateral to hemispheric lesion due to false localizing
87
Decerebrate posturing associated with herniation
compression of the midbrain, central and uncal herniation
88
Hypertension. bradycardia associated with herniation
compression of the medulla, central, uncal, and cerebellar (tonsillar)
89
Abnormal breathing patterns associated with herniation
compression of the pons and medulla. Central, uncal, and cerebellar (tonsillar)
90
Posterior cerebral artery infarction associated with herniation
vascular compression, uncal herniation
91
Anterior cerebral artery infarction associated with herniation
vascular compression, Subfalcine (cingulate)

Clinical Medicine III (5 decks)

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