Case Vignettes in Neurology

PATIENT CASE STUDIES

Case 43 3/18/99 Spells & TIAs
Case discussion A 40 year old male hypertensive, non insulin dependent diabetic awoke with weakness of the left side of the body and was admitted to the hospital. He gave a history of a transient episode of mild weakness of the right side of the body occurring a week before that had resolved after 3-4 hours for which he did not seek medical attention. He gave a history of nocturia, thirst and weight loss for the prior one year, and had recently been diagnosed with diabetes. There was a family history of diabetes His medications included hydrochlorthiazide and glyburide. On examination, 2 hours after awakening, the blood pressure was 170/90, pulse 110, temperature 36.5 C. General examination was unremarkable. On neurological examination he was awake, anxious, and poorly attentive. He was oriented to person and UCDMC, Sacramento but was unsure of the month and day. Speech was fluent with good comprehension, repetition and naming. He was able to follow three step appendicular commands. On cranial nerve examination the fundi were benign and there was a right sided facial palsy sparing the forehead. On motor examination weakness was detected in the right upper and lower extremities, with 4/5 strength in the deltoid, triceps, wrist and finger extensors, hip flexors, knee flexors and foot dorsiflexors. Cerebellar testing was impaired by weakness on the right side but otherwise normal. Sensory examination was normal. DTRs were brisk throughout, slightly brisker on the right side. The right plantar reflex was extensor and the left was flexor.
Summarize the Case in 1-2 sentences. This patient is a 40 year old hypertensive, poorly controlled diabetic with a history of a transient episode of right hemiparesis a week earlier who awoke with a new onset of right hemiparesis, including right lower facial palsy, and characteristic UMN lesion symptoms (+ babinski on the right side, brisk DTRâs on the right side). Sensory and cerebellar exams are normal, however patient is poorly attentive with some loss of orientation. His current medications are hydrochlorthiazide and glyburide. good Discuss lesion localization on the basis of the physical examination. Pure motor right hemiparesis Ð Left internal capsule Mild confusion Ð cortical lesion good Discuss underlying pathogenesis on the basis of clinical course. Recurrent onset suggests a toxic, metabolic, or vascular etiology. good Indicate one likely clinical diagnosis. List (or classify) alternative diagnoses. Hypoglycemia secondary to overuse of diabetic medication. good Indicate 2 ancillary tests that would assist in confirming or refuting the clinical diagnosis. Indicate the test results that would confirm the clinical diagnosis. Blood Glucose - under 70 mg/dl will show hypoglycemia. Lower concentrations may indicate levels associated with changing mental status and neurological deficits. MRI to refute diagnosis by evidence of infarction. good; note that hypoglycemia can lead to infarction if not reversed Indicate complications of the disease and ancillary tests that would help evaluate them. a. Central nervous system (CNS) symptoms worsen in severity with severe or prolonged hypoglycemia and include dizziness, headache, clouding of vision, blunted mental acuity, loss of fine motor skill, confusion, abnormal behavior, convulsions, and loss of consciousness. b. Autonomic symptoms - sweating, tremor, tachycardia, anxiety, and hunger - check vitals c. Permanent neurological deficit - neuro exam/imaging study d. Death good Discuss how the underlying pathophysiology is relevant in the management of this patient. Acute management of the patient is IV glucose. In patients beginning diabetic therapy, it is important to modulate the dosage and frequency of the prescription. As with this patient, with inadequate follow up, symptoms of hypoglycemia may go unchecked for long periods of time, leading to CNS changes. Subsequently, the management of this patient would include home blood glucose checks (Accucheck), as well as, careful monitoring of the use of some antidiabetic drugs that have a long duration of action and high potency (e.g. glyburide and glipizide). The hypoglycemic states can best be understood as derangements of normal fuel metabolism. Under ordinary circumstances, energy needs are met by exogenous substrate in the form of food. Oxidation of the constituent molecules of food to carbon dioxide and water generates adenosine triphosphate (ATP), the principal high-energy compound of the body. Subsequently, without ATP, the ion pumps in the membrane of cells will not be able to function, leading to an influx of sodium, calcium (and other ions) and water. This situation will eventually lead to free radical formation, intracellular edema, necrosis, and electrical failure. Hypoglycemia is especially dangerous in the brain because glucose is the primary energy substrate. Its absence, like that of oxygen, produces deranged function, tissue damage, and death if the deficit is prolonged. The brain is vulnerable to hypoglycemia because it cannot utilize circulating free fatty acids as an energy source, in contrast to other tissues. In cases of extreme hypoglycemia, not only is confusion seen, but also focal deficits may be apparent (as in this patient) due to the different metabolic needs of various parts of the brain. good, on the long side

Case 43 3/18/99 Spells & TIAs

Case discussion
A 40 year old male hypertensive, non insulin dependent diabetic awoke with weakness of the left side of the body and was admitted to the hospital. He gave a history of a transient episode of mild weakness of the right side of the body occurring a week before that had resolved after 3-4 hours for which he did not seek medical attention. He gave a history of nocturia, thirst and weight loss for the prior one year, and had recently been diagnosed with diabetes. There was a family history of diabetes
His medications included hydrochlorthiazide and glyburide.

On examination, 2 hours after awakening, the blood pressure was 170/90, pulse 110, temperature 36.5 C. General examination was unremarkable. On neurological examination he was awake, anxious, and poorly attentive. He was oriented to person and UCDMC, Sacramento but was unsure of the month and day. Speech was fluent with good comprehension, repetition and naming. He was able to follow three step appendicular commands. On cranial nerve examination the fundi were benign and there was a right sided facial palsy sparing the forehead. On motor examination weakness was detected in the right upper and lower extremities, with 4/5 strength in the deltoid, triceps, wrist and finger extensors, hip flexors, knee flexors and foot dorsiflexors. Cerebellar testing was impaired by weakness on the right side but otherwise normal. Sensory examination was normal. DTRs were brisk throughout, slightly brisker on the right side. The right plantar reflex was extensor and the left was flexor.

Summarize the Case in 1-2 sentences.

This patient is a 40 year old hypertensive, poorly controlled diabetic with a history of a transient episode of right hemiparesis a week earlier who awoke with a new onset of right hemiparesis, including right lower facial palsy, and characteristic UMN lesion symptoms (+ babinski on the right side, brisk DTRâs on the right side). Sensory and cerebellar exams are normal, however patient is poorly attentive with some loss of orientation. His current medications are hydrochlorthiazide and glyburide.

good

Discuss lesion localization on the basis of the physical examination.

Pure motor right hemiparesis Ð Left internal capsule Mild confusion Ð cortical lesion

good

Discuss underlying pathogenesis on the basis of clinical course.

Recurrent onset suggests a toxic, metabolic, or vascular etiology.

good

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

Hypoglycemia secondary to overuse of diabetic medication.

good

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

Blood Glucose - under 70 mg/dl will show hypoglycemia. Lower concentrations may indicate levels associated with changing mental status and neurological deficits.

MRI to refute diagnosis by evidence of infarction.

good; note that hypoglycemia can lead to infarction if not reversed

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

a. Central nervous system (CNS) symptoms worsen in severity with severe or prolonged hypoglycemia and include dizziness, headache, clouding of vision, blunted mental acuity, loss of fine motor skill, confusion, abnormal behavior, convulsions, and loss of consciousness.

b. Autonomic symptoms - sweating, tremor, tachycardia, anxiety, and hunger - check vitals

c. Permanent neurological deficit - neuro exam/imaging study

d. Death

good

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

Acute management of the patient is IV glucose. In patients beginning diabetic therapy, it is important to modulate the dosage and frequency of the prescription. As with this patient, with inadequate follow up, symptoms of hypoglycemia may go unchecked for long periods of time, leading to CNS changes. Subsequently, the management of this patient would include home blood glucose checks (Accucheck), as well as, careful monitoring of the use of some antidiabetic drugs that have a long duration of action and high potency (e.g. glyburide and glipizide).

The hypoglycemic states can best be understood as derangements of normal fuel metabolism. Under ordinary circumstances, energy needs are met by exogenous substrate in the form of food. Oxidation of the constituent molecules of food to carbon dioxide and water generates adenosine triphosphate (ATP), the principal high-energy compound of the body. Subsequently, without ATP, the ion pumps in the membrane of cells will not be able to function, leading to an influx of sodium, calcium (and other ions) and water. This situation will eventually lead to free radical formation, intracellular edema, necrosis, and electrical failure.

Hypoglycemia is especially dangerous in the brain because glucose is the primary energy substrate. Its absence, like that of oxygen, produces deranged function, tissue damage, and death if the deficit is prolonged. The brain is vulnerable to hypoglycemia because it cannot utilize circulating free fatty acids as an energy source, in contrast to other tissues. In cases of extreme hypoglycemia, not only is confusion seen, but also focal deficits may be apparent (as in this patient) due to the different metabolic needs of various parts of the brain.

good, on the long side