Radiology Interactive Case 9

Radiology Interactive Case 9 Neurology A Section C Macadangdang, Panganiban, A., Panganiban, J., Paredes, Pasana, Pau, Paulino, Payuyo, Pelino, Perez

78 yo right handed female from Cavite

Chief Complaint: Alteration in level of sensorium

History of Present Illness

Past Medical History • (+) Hypertension Stage 2 with Atrial Fibrillation – poor compliance with her medication

• (+) DM Type 2, uncontrolled

Personal and Social History • Non smoker • Non alcoholic beverage drinker

Pertinent Physical Examination • BP 140/100 mm Hg CR/PR 80s irregularly irregular RR 24 • No carotid bruit • Symmetrical chest expansion, clear breath sounds • Adynamic precordium, AB 6th LICS MCL, (+) holosystolic murmurs at the apex

Neurologic Examination • Eye opening to name calling but with difficulty in maintaining wakefulness, incomprehensible words, can follow simple commands • Pupils isocoric 2-3 mm ERTL • EOMs: conjugate; no preferential gaze • (+) corneal reflex, bilateral • Can raise eyebrows equally, shallow left nasolabial fold • Tongue deviated to the left • Motor Exam: unable to move her left extremities (0/5) • Numbness on the left extremities • Cerebellum: difficult to assess at this time • Babinski, left • No nuchal rigidity

Glasgow Coma Scale •

Eye opening 4 – spontaneous eye opening 3 – eyes open to speech 2 – eyes open to pain 1 – no eye opening

•

Verbal response

GCS Score: 11

5 – alert and oriented 4 – confused, yet coherent; can speak coherently 3 – garbled phrases; inappropriate words 2 – incomprehensible sounds 1 – no sounds

•

Motor response 6 – full obeys commands 5 – responds to painful stimuli 4 – withdraws from noxious stimuli or pain; not as purposeful as in 5 3 – abnormal reaction to stimuli 2 – unnatural posturing; head arched back, arms bend in toward chest, fists clenched, legs extended 1 – no response

Salient Features – Pertinent Positive Subjective • 78 yo • Slurring of speech • Left-sided weakness • Vomiting • Drowsy

Objective • • • • • • • • • •

(+) Hypertension Stage 2 with Atrial Fibrillation, poor compliance (+) DM Type 2, uncontrolled BP 140/100 mm Hg CR/PR 80s irregularly irregular AB 6th LICS MCL, (+) holosystolic murmurs at the apex GCS score: 11 shallow left nasolabial fold Tongue deviated to the left left extremities – MMT: 0/5, numbness (+) left Babinski

Salient Features – Pertinent Negative Subjective • Non smoker • Non alcoholic beverage drinker

Objective • No nuchal rigidity

Lesion LEVELIZE:

cerebral cortex LATERALIZE:

right side LOCALIZE: CT and MRI findings

Working Diagnosis: Stroke

Stroke a.k.a. cerebrovascular accident A symptom complex resulting from cerebral hemorrhage or from embolism or thrombosis of the cerebral vessels, characterized by alterations in consciousness, seizures, and development of focal neurologic deficit Blakinston’s Pocket Medical Dictionary, 4th edition

Risk Factors Modifiable • • • • • • • • • •

Non-Modifiable

High blood pressure Cigarette smoking Diabetes mellitus Carotid or other artery disease Atrial fibrillation Other heart disease Sickle cell disease High blood cholesterol Poor diet Physical inactivity and obesity

• • • • •

Age Family history Race Sex Prior stroke, TIA or heart attack

American Heart Association

14 http://www.americanheart.org/presenter.jhtml?identifier=4716

Types of Stroke Type

Onset

Precedi ng TIAs (%)

Thrombotic

% of all stroke s 40

May be gradua l

50

Embolic

30

Lacunar

20

Hemorrhagi c

10

Altered Mental Status (%) 5

MRI or CT Scan

Other Features

Ischemic infarction

Carotid bruit, stroke during sleep

Sudden 10

1

Superficial (cortical) infarction

May be gradua l

0

Small, deep infarction

Underlying heart disease, peripheral emboli or strokes in different vascular Pure motor or territories pure sensory

30

Sudden 5

Medical Secrets by Anthony Zollo, Jr.

stroke 25

Hyperdense mass

Nausea and vomiting, decreased mental status

16

Embolic Stroke • Most often diagnosed in patients with an underlying cardiac disease • Abrupt in onset, with more rapid resolution, and tend to cause smaller neurologic deficits than thrombotic stroke • Embolus travel in the arterial stream until it reaches a blood vessel to occlude it • Cortical deficits, such as aphasia 17

Radiology • CT scan • Magnetic Resonance Imaging (MRI) – Magnetic Resonance Angiograph

Computed Tomography (CT) • method of choice for the assessment of acute ischemic injury • recommended imaging modality for initial evaluation of patients suspected of having a stroke • Sensitive for detection of calcifications and acute hemorrhage • Rapid, widely available, low cost, non-invasive, short study time

GILMAN, C., 1998. Imaging the Brain. The New England Journal of Medicine. 332: 812-820 19

Computed Tomography (CT) • Can not detect an infarction in the first three hours after the onset of symptoms • Hyperdensity of a major cerebral vessel-important sign of vessel thrombosis • Limited capacity to show vascular lesions in the brainstem, cerebellum and small deep ischemic infarctions GILMAN, C., 1998. Imaging the Brain. The New England Journal of Medicine. 332: 812-820 20

Normal CT Scan

CT Scan

Early CT Changes in Ischemic Stroke • Hypodensity • Obscured insular ribbon • Dense MCA sign • Loss of gray-white interface • Loss of sulci • Mass effect 23

CT Scan

*HEWKO, C., 2004. Acute ischemic stroke--swift assessment & quick action produce optimal outcomes. JAAPA,

24

Non-hemorrhagic

Hemorrhagic

GILMAN, C., 1998. Imaging the Brain. The New England Journal of Medicine. 332: 812-820

Computed Tomography (CT) • Loss of Insular Ribbon Sign – insular ribbon • is an area of extreme gray-white differentiation that is readily examined on the CT scan • between the Sylvian fissure and the basal ganglia • supplied by small perforating branches of the MCA • appears as a thin white line (gray-matter) adjacent to a darker gray subcortical area (white-matter)

Loss of Insular Ribbon

FLACKE, S. et al. 1999. Middle Cerebral Artery (MCA) Susceptibility Sign at Susceptibility-based Perfusion MR Imaging: Clinical Importance and Comparison with Hyperdense MCA Sign at CT. Radiology. 2000; 215:476-482.

Computed Tomography (CT) • Hyperdense MCA sign: – major occlusion of the vessel with thrombus formationhypoperfusion – 98 % specificity, 50% sensitivity – also correlates with final stroke severity

Hyperdense MCA Sign

FLACKE, S. et al. 1999. Middle Cerebral Artery (MCA) Susceptibility Sign at Susceptibility-based Perfusion MR Imaging: Clinical Importance and Comparison with Hyperdense MCA Sign at CT. Radiology. 2000; 215:476-482.

Hyperdense MCA Sign

Computed Tomography (CT) • The earliest signs of infarction are usually subtle and include: – loss of gray-white differentiation at the cortical-subcortical junction – basal ganglia and sulcal effacement

• These signs appear within 6 hours of onset in over 80% of patients with MCA infarctions, but are often less obvious when infarcts affect other territories

Loss of Gray-White Interface

American College of Physicians, Inc. 2006. Internal Medicine Essentials for Clerkship Students. Accessed from: acponline.org/essentials

Computed Tomography (CT) • Hypodensity (edema) and mass effect develop next – if present in more than 50% of the MCA territory within 24 hours of onset correlate with early neurologic deterioration and death

Computed Tomography (CT) • Mass effect – Compression of CSF spaces and asymmetry of cortical sulci

Mass Effect

American College of Physicians, Inc. 2006. Internal Medicine Essentials for Clerkship Students. Accessed from: acponline.org/essentials

35

CT scan of patient 9 hours after the onset of symptoms

CT Scan of Patient

Contrastenhanced CT scan of patient 9 hours after the initial noncontrast CT scan

Contrast-enhanced CT of Patient

Contrast-enhanced CT of Patient

Early CT Changes in Ischemic Stroke • Hypodensity • Obscured insular ribbon • Dense MCA sign • Loss of gray-white interface • Loss of sulci • Mass effect 41

CT Scan of Patient

CT Scan of Patient • Hypodensity • Loss of gray-white interface • Loss of sulci • Mass effect

43

Obscured Insular Ribbon

Contrast-enhanced CT of Patient

Hyperdense MCA Sign

Magnetic Resonance Imaging (MRI) • More sensitive than CT to the early pathologic changes of ischemic infarction • Relatively insensitive for detecting early signs of cerebral ischemia • Superior in detecting brain edema, small cortical and subcortical infarcts, as well as those in the brainstem and cerebellum • more sensitive and specific than CT for identifying infarct location, size, and age • Longer time to perform • More expensive than CT GILMAN, C., 1998. Imaging the Brain. The New England Journal of Medicine. 332: 812-820 47

Magnetic Resonance Imaging (MRI) • Diffusion-weighted imaging (DWI) – detects subtle changes in the diffusion of water molecules within ischemic tissue and can accurately identify areas of ischemia – within minutes of onset and may persist for weeks – for acute ischemia, sensitivity: >90% and specificity: >95%

Magnetic Resonance Imaging (MRI) • Perfusion-weighted imaging (MRI) – Tracks a gadolinium bolus into the brain parenchyma – PWI detects areas of hypoperfusion or “at risk” tissue that is still viable

DWI/PWI Mismatch • Subtract DWI signal (infarct core) from PWI signal • DWI/PWI mismatch is the hypoperfused area that may still be viable (ISCHEMIC PENUMBRA) – Large mismatch: reperfusion may benefit even beyond the 3-hour t-PA window – No mismatch: there may be little benefit to thrombolytic therapy, even within 3hour period

DWI MRI 35 minutes after symptom onset

Magnetic Resonance Angiography (MRA) • a sequence which enables the evaluation of cervical and cerebral arteries • a noninvasive test that can be performed without contrast injection and provides 3D images of the vascular system

Catheter Angiography • best parameter to document stroke • invasive, potentially high-risk procedure  • although this test has largely been supplanted by MR angiography and CT angiography, it remains the gold standard in the evaluation of intracranial, extracranial, and spinal vascular lesions. • performed routinely in patients with subarachnoid hemorrhage or unexplained intracranial hemorrhage. • occasionally performed to evaluate the intracranial blood vessels for vasculitis

Catheter Angiography • Major complications: – Bleeding and thrombosis at the puncture site – Vascular dissections at any level – Small plaques dislodged by the catheter and small clots forming around the catheter tip may embolize, leading to cerebral or spinal infarction • Major risk factors for complications: – Age − Hypertension – Diabetes − Peripheral vascular disease – Coronary artery disease 

Catheter Angiography • Advantages: – extremely high spatial resolution – remains the gold standard in the evaluation of the vascular system.  • Disadvantages: – procedure is long and often requires serious sedation • When to Order: – Subarachnoid or parenchymal hemorrhage – Vasculitis – Spinal vascular malformation

Diagnosis: Thromboembolic Stroke

Pathophysiology Cerebral ischemia is caused by a reduction in blood flow that lasts longer than several seconds. A stroke, or cerebrovascular accident, is defined by this abrupt onset of a neurologic deficit that is attributable to a focal vascular cause. Most cerebrovascular diseases are manifest by the abrupt onset of a focal neurologic deficit, as if the patient was “struck by the hand of God”. Harrison’s Principles of Internal Medicine, 16th Ed.

59

Blood Flow • 0 = death of brain within 4 to 10 minutes • <16-18 ml/100g tissue/min = infarction within an hour • <20 mL/100g tissue/min = ischemia w/o infarction (unless prolonged for hours or days) *If blood flow is restored prior to a significant amount of cell death, the patient may experience only transient symptoms, i.e. TIA Harrison’s Principles of Internal Medicine, 16th Ed. 60

Penumbra • Heterogeneity in brain injury has been documented in an infarcted zone. • Blood flow to an infarcted zone is said to have: – A. a central region or core of very low flow that results in rapid cell demise and – B. a peripheral penumbra where decline in flow is more moderate and cell death

Penumbra • The penumbra is thought to represent salvageable tissues that may go on to infarction. • If blood flow is normalized at an adequate time, the brain cells will normalize.

63

Cell Death Pathways 1. Necrotic pathway – Rapid cellular cytoskeleton breakdown

2. Apoptotic pathway – Cells become programmed to die

64

Harrison’s Principles of Internal Medicine, 16th Ed.

65

Thank you!!!

Necrotic Pathway ischemia

↓ glucose in neurons

agonize postsynaptic glutamate receptors

glutamate release from synaptic terminals

↑ intracellular calcium

depolarization of neurons

proteolysis

necrosis

↓ ATP production by mitochondria

membrane ion pumps stop functioning

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Management PHARMACOLOGIC 1. Reverse or lessen the amount of tissue infarction (initial management)

1. Reduce the risk of further strokes and other vascular problems

• by optimizing cerebral perfusion in the surrounding ischemic penumbra 1. Reperfuse the tissues (thrombolytics and vasodilators) 2. Prevent further thrombotic events (antiplatelets and anticoagulation) 3. Maintain blood pressure • plan for secondary prophylaxis (drugs)

Management NON- PHARMACOLOGIC

1. Reduce the patient’s disability and handicap through rehabilitation (physical, occupational, and speech therapy consultation) 2. Plan for secondary prophylaxis (risk factor modifications) 3. Prevent the common complication of bedridden patients