Case Vignettes in Neurology

PATIENT CASE STUDIES

Case 41 3/17/99 Coma
Case discussion This 66-year-old, right-handed, black male was admitted to UCDMC on 4/24195 from Vaca Valley Hospital after a series of events that began when he fell and hit his head four days prior to admission, developed severe neck and back pain, and eventually became very poorly responsive. His neurologic history began in 1993 when he suffered the first of several cerebral infarcts that resulted in left visual field loss, transient left hemiparesis and in early 1995, mild right hemiparesis and dysphasia. On 4/20/95, he fell from bed, struck his head and developed sudden onset of very severe headache, neck pain and back pain. CT scan at Vaca Valley Hospital showed only the previous cerebral infarcts. The back pain subsided with intramuscular non-steroidal anti-inflammatory medication (Toradol), but recurred over the next two days. On 4/23/95, due to increasing back and neck pain, he was examined again at Vaca Valley Hospital where he was noted to have a left frontal laceration, confusion and posterior cervical tenderness. He was transferred at that time to UCDMC. Past medical history is significant for multiple cerebral infarcts (assumed to be secondary to embolization of left ventricular clot) diabetes, congestive heart failure, hypertension, chronic renal insufficiency, dementia, ventricular arrhythmias, hyperlipidemia, sickle cell trait and dilated cardiomyopathy. Medications included Coumadin to prevent left ventricular thromboemboli. Examination at UCDMC on 4/24/95 revealed mild nuchal rigidity, confusion and disorientation, slow incomprehensible speech, but no localizing neurologic deficit. Pathologic Case Correlate: Neuropath Case X1
Summarize the Case in 1-2 sentences. 66 y.o male presents with subacute progressive HA, Neck pain, back pain, confusion, disorientation, and dysarthria. PMH significant for multiple cerebral infarcts. you left out the injury and that he became poorly responsive (comatose), and his PMH for cardiac problems, diabetes, hypertension, sickle cell disease Discuss lesion localization on the basis of the physical examination. Meninges, Diffuse cortical involvement, Left temporal Lobe indicate why e.g meninges (neck stiffness), cortical involvement (confusion) not decreased level of consciousness may be secondary to diffuse (bilateral) cortical dysfunction or brain stem involvement. I am not sure why you say left temporal lobe; also you need to inicate the possible localization of the prior cerebral infarcts Discuss underlying pathogenesis on the basis of clinical course. Sub-acute Progressive suggests metablolic, infectious, autoimmune onset seems very sudden to me, after the fall, with subsequent acute or subacute progresion Indicate one likely clinical diagnosis. List (or classify) alternative diagnoses. Saccular ruptured aneurysm Alternative diagnoses include Meningitis, thromboembolitic infarcts, ischemic acidosis OK; since onset was sudden vascular causes including other causes of hemorrhage are important Indicate 2 ancillary tests that would assist in confirming or refuting the clinical diagnosis. Indicate the test results that would confirm the clinical diagnosis. Repeat a CT - expect to see blood diffusely present in sub-arachnoid space LP- expect to see blood tinged CSF ok Indicate complications of the disease and ancillary tests that would help evaluate them. Rerupture- four vessel Angiography DVT-Venogram no comment Discuss how the underlying pathophysiology is relevant in the management of this patient. Ventriculostomy- to decrease intracranial pressure (ICP) secondary to hydrocephalus Ca channel antagonist- Nimodipine to decrease vasospasms Microsurgical clips to treat ruptured aneurysm Short term reduction of Coumadin to decrease aneurysmal leakage Glucocorticoids to decrease head/neck pain Stool softener to decrease valsalva with bowel movements to prevent increase in ICP Hyperventilation and Mannitol to decrease ICP for SAH need to discuss pathophysiology of vasospasm

Case 41 3/17/99 Coma

Case discussion

This 66-year-old, right-handed, black male was admitted to UCDMC on 4/24195 from Vaca Valley Hospital after a series of events that began when he fell and hit his head four days prior to admission, developed severe neck and back pain, and eventually became very poorly responsive.

His neurologic history began in 1993 when he suffered the first of several cerebral infarcts that resulted in left visual field loss, transient left hemiparesis and in early 1995, mild right
hemiparesis and dysphasia. On 4/20/95, he fell from bed, struck his head and developed sudden onset of very severe headache, neck pain and back pain. CT scan at Vaca Valley Hospital showed only the previous cerebral infarcts. The back pain subsided with intramuscular non-steroidal anti-inflammatory medication (Toradol), but recurred over the next two days. On 4/23/95, due to increasing back and neck pain, he was examined again at Vaca Valley Hospital where he was noted to have a left frontal laceration, confusion and posterior cervical tenderness. He was transferred at that time to UCDMC.

Past medical history is significant for multiple cerebral infarcts (assumed to be secondary to embolization of left ventricular clot) diabetes, congestive heart failure, hypertension, chronic renal insufficiency, dementia, ventricular arrhythmias, hyperlipidemia, sickle cell trait and dilated cardiomyopathy.

Medications included Coumadin to prevent left ventricular thromboemboli.

Examination at UCDMC on 4/24/95 revealed mild nuchal rigidity, confusion and disorientation, slow incomprehensible speech, but no localizing neurologic deficit.

Pathologic Case Correlate: Neuropath Case X1

Summarize the Case in 1-2 sentences.

66 y.o male presents with subacute progressive HA, Neck pain, back pain, confusion, disorientation, and dysarthria. PMH significant for multiple cerebral infarcts.

you left out the injury and that he became poorly responsive (comatose), and his PMH for cardiac problems, diabetes, hypertension, sickle cell disease

Discuss lesion localization on the basis of the physical examination.

Meninges, Diffuse cortical involvement, Left temporal Lobe

indicate why e.g meninges (neck stiffness), cortical involvement (confusion) not decreased level of consciousness may be secondary to diffuse (bilateral) cortical dysfunction or brain stem involvement. I am not sure why you say left temporal lobe;

also you need to inicate the possible localization of the prior cerebral infarcts

Discuss underlying pathogenesis on the basis of clinical course.

Sub-acute Progressive suggests metablolic, infectious, autoimmune

onset seems very sudden to me, after the fall, with subsequent acute or subacute progresion

Indicate one likely clinical diagnosis. List (or classify) alternative diagnoses.

Saccular ruptured aneurysm

Alternative diagnoses include Meningitis, thromboembolitic infarcts, ischemic acidosis

OK; since onset was sudden vascular causes including other causes of hemorrhage are important

Indicate 2 ancillary tests that would assist in confirming or refuting the clinical diagnosis. Indicate the test results that would confirm the clinical diagnosis.

Repeat a CT - expect to see blood diffusely present in sub-arachnoid space
LP- expect to see blood tinged CSF

Indicate complications of the disease and ancillary tests that would help evaluate them.

Rerupture- four vessel Angiography
DVT-Venogram

no comment

Discuss how the underlying pathophysiology is relevant in the management of this patient.

Ventriculostomy- to decrease intracranial pressure (ICP) secondary to hydrocephalus
Ca channel antagonist- Nimodipine to decrease vasospasms
Microsurgical clips to treat ruptured aneurysm
Short term reduction of Coumadin to decrease aneurysmal leakage
Glucocorticoids to decrease head/neck pain
Stool softener to decrease valsalva with bowel movements to prevent increase in ICP
Hyperventilation and Mannitol to decrease ICP

for SAH need to discuss pathophysiology of vasospasm