Hospital Practice

ISSN: 2154-8331 (Print) 2377-1003 (Online) Journal homepage: http://www.tandfonline.com/loi/ihop20

Dysarthria and a Numb Hand In an Elderly Woman
Clifford L. McDonald, Nafeesa F. Mahmood & Kenneth F. Grant
To cite this article: Clifford L. McDonald, Nafeesa F. Mahmood & Kenneth F. Grant (1992)
Dysarthria and a Numb Hand In an Elderly Woman, Hospital Practice, 27:1, 71-74, DOI:
10.1080/21548331.1992.11705343
To link to this article: http://dx.doi.org/10.1080/21548331.1992.11705343

Published online: 17 May 2016.

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Date: 16 June 2016, At: 16:23

The Problem Patient

Dysarthria and a Nun1b Hand
In an Elderly Won1an
CLIFFORD L. McDONALD. NAFEESA F. MAHMOOD, and KENNETH F. GRANT

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Blodgett Memorial Medical Center, Grand Rapids

Case Presentation
A 74-year-old woman with a history of coronary artery disease
presented with progressive, intermittent symptoms of slurred
speech and numbness of the
right hand for the past week. She
was taking butalbital-acetaminophen several times a day for severe bitemporal headaches.
She had been hospitalized five
weeks earlier with right-hand
weakness and clumsiness. ACT
scan at that time revealed infarction of the right caudate nucleus
and of the left parietal lobe. An
echocardiogram showed no evidence of chamber enlargement,
significant valvular disease, or
mural thrombi. Carotid duplex
scanning showed no evidence
of hemodynamically significant
stenosis, and an ECG was negative for arrhythmia.
Despite these studies, it was

At the time the patient was seen, Dr.
McDonald was an Attending Internist,
Dr. Mahmood was a Resident, and
Dr. Grant was an Attending Physician, Pathology Department, Blodgett
Memorial Medical Center, Grand
Rapids.

felt that the patient's cerebral infarcts had an embolic source,
and warfarin was prescribed at
discharge. Prothrombin time
three weeks before her current
presentation was within the therapeutic range. By all accounts,
the patient was compliant with
her medications and had not exceeded her prescribed warfarin
dosage. She denied taking aspirin or other nonsteroidal antiinflammatory drugs.
On physical examination, the
patient had slightly reddened
cheeks but was not in apparent
distress. Vital signs were normal.
She had right facial weakness
with sparing of the eyebrow.
Heart sounds were regular with
an S 4 present but no rub or murmur. Other than the facial weakness, her cranial nerves appeared intact. She had slightly decreased right-hand grip
strength and some numbness in
the right thumb and index finger. Her speech exhibited mild
dysarthria, probably related
to her facial weakness. The remainder of the examination was
normal.
A CT scan performed after her

admission was interpreted as
showing evidence of a small,
probably early, infarct in the left
posterior parietal region without
hemorrhage. The patient's prothrombin time was elevated at
33.5 seconds (control, 12).
Other laboratory data were remarkable for a hemoglobin of 17,
hematocrit 49 .9, and white blood
cell count 11.4 with a differential
of 89 segs, 5 bands, 4 lymphs, 1
mono, and 1 eosinophil. A platelet count performed manually
was found to be 1,126,000. MCV
was 89 fl. On her previous admission, her hemoglobin had been
15.6, hematocrit 45.1, and platelet count 987,000.
It was felt that the patient's
neurologic symptoms could easily be explained by a hyperviscosity syndrome or platelet thrombi
related to her profound thrombocythemia. Hematology and
neurology consultations were obtained. Arterial blood gases,
leukocyte alkaline phosphatase,
and erythropoietin levels were
drawn to better delineate what
was thought to be a myeloproliferative syndrome, probably
polycythemia vera.
The blood chemistries were
Hospital Practice January 15. 1992

71

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normal, and the patient had a Po 2
of 7 4 mm Hg on room air. A red
blood cell mass study and bone
marrow biopsy were considered
for future workup. The patient
was admitted for observation
and given 2 units of fresh frozen
plasma to correct her prothrombin time.
During the night the patient
had some worsening of her neurologic status, with development
of a true aphasia that progressed
along with the right-sided weakness. By morning she had evidence of both expressive and receptive aphasia, left tongue deviation, and a right upgoing plantar
reflex. She was given 10 grains of
aspirin, and plans were initiated
for plateletpheresis.
After an initial plateau at this
level of deficit, the patient showed
further signs of rapid neurologic
deterioration with progressive
loss of consciousness, and she
became unresponsive to painful
stimuli within a few hours. Repeat prothrombin time remained
elevated at 20.2 seconds. Arepeat CT scan revealed acute bilateral parietal subdural hematomas with considerable mass
effect. There was also an intracerebral hematoma at the occipitoparietal junction on the left at
the site of the earlier infarct. Evidence of tonsillar herniation also
appeared to be present.
The patient was intubated and
hyperventilated, and steroids
were given intravenously. By this
time the patient had lost all signs
ofbrainstem function, such that
neurosurgical intervention was
deemed unfeasible. The patient
died approximately 24 hours
after admission.
Gross findings on autopsy
confirmed the presence of bilateral subdural hematomas along
with an intracerebral hematoma
72

Hospital Practice January 15. 1992

in the occipitoparietal region of
the left cerebral hemisphere.
There were also gross findings in
the brain confirming tonsillar
herniation. The other significant
finding was a moderately enlarged spleen weighing 450 gm.
On review of microscopic sections, the spleen revealed characteristic pooling of platelets in
the splenic sinuses. There was
no evidence of splenic extramedullary hematopoiesis. The
bone marrow revealed 80% cellularity. There was hyperplasia
of all three cell lines with the
megakaryocytes being most
prominent, having atypical nuclei. Sections of the left middle
cerebral artery demonstrated a
90% occlusion with an organizing thrombus 2 to 3 em from
its origin. In addition to being
severely narrowed, the lumen
contained fresh fibrin and
platelet deposits attached to the
endothelium.

The Case in Context
According to one recent review, hematologic disorders may
play an etiologic role in up to 7%
of all cerebral infarcts, depending on the population studied.
Higher incidences are seen in series of younger patients (<50
years) who have infarcts. These
hematologic disorders include
diseases involving clotting factors and their inhibitors, such as
antithrombin III deficiency, protein C and S deficiencies, and the
presence oflupus anticoagulant.
Also included are disorders involving formed blood elements,
such as polycythemia vera, sickle cell anemia and trait, sickle
cell-hemoglobin C disease, and
essential thrombocythemia.
Our patient appears to have
had one of the myeloproliferative
disorders, with clinical evidence
dating back to her first admis-

sian with stroke. She could have
had either PCV with marked
thrombocythemia or essential
thrombocythemia. The definitive study that could have distinguished these would have been
a red cell mass index, which was
not performed before her death.
The findings in the marrow are
usually not considered specific
to essential thrombocythemia
versus PCV with marked thrombocythemia. Without the finding of hypoxia or an elevated
erythropoietin level, most cases
of secondary polycythemia are
ruled out.
Polycythemia vera is known to
cause excessive thrombosis as
well as bleeding. According to a
review by Schafer, thrombosis
appears to be more prominent
than bleeding in PCV, whereas
essential thrombocythemia is
more commonly associated with
excessive bleeding. In addition,
PCV causes CNS symptoms
through heightened viscosity,
with global cerebral dysfunction
such as mental slowness, lethargy, dizziness, tinnitus, and
headache. It is therefore not
surprising that cerebral thrombosis is a particularly prominent
complication among patients
with PCV. An increased hematocrit is associated with decreased cerebral blood flow, a
relationship that applies even
within the normal range of hematocrits. It is therefore clearly
of benefit to perform phlebotomy in a patient with neurologic
symptoms and a markedly elevated hematocrit.
Although the relationship between increased hematocrit and
poor cerebral perfusion and
thrombosis in PCV seems clear,
the association of the platelet
count level with the incidence of
thrombosis or bleeding in essen(continues)

THROMBOSIS

1992
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(continued}

tial thrombocythemia is more
controversial. Several studies
found bleeding to be most common, whereas others suggest
that thrombosis is the greater
threat, especially cerebrovascular bleeding. Several small series
of studies report cases similar to
ours, with cerebral infarct as the
initial manifestation of essential thrombocythemia.
Whatever the more common
complication-thrombosis or
bleeding-there are several functional deficits in the platelets of
patients with essential thrombocythemia. These include abnormal platelet morphology, acquired storage pool disease,
platelet membrane abnormalities, and abnormal arachidonic
acid metabolism. Awareness of
these deficits has intensified the
controversy over whether aspirin
or other platelet inhibitors
should be given to patients with
essential thrombocythemia and
thrombotic sequelae. Although
patient data from a multi-institutional PCV study group suggested a consistent benefit in
thrombotic CNS symptoms
among patients given aspirin,
other investigators have been
reluctant to recommend this rou-

tinely. Indeed, aspirin has been
shown to prolong the bleeding
time significantly in patients
with essential thrombocythemia,
compared with normal controls.
Our patient was at greater risk
ofhemorrhage, having been given
warfarin for what was mistakenly
believed to be an embolic cause
of bilateral infarcts seen on her
initial CT scan. Despite a markedly prolonged prothrombin time
and her more than adequately inhibited coagulation, she presented with a cerebral infarct related
to her platelet and viscosity abnormalities. Her impaired coagulation could in fact account for
her subsequent intracerebral
hemorrhage into an initially
bland infarct. However, it does
not seem to account as well for
the development of the apparently spontaneous bilateral subdural hematomas.
Despite controversy over exact
mechanisms and measures to
prevent neurologic sequelae in
myeloproliferative disorders,
this case demonstrates their potential to cause life-threatening
CNS sequelae. This possibility
should be considered in the evaluation of the patient with new
onset of a thrombotic or hemorrhagic CNS phenomenon.
0

Selected Reading

Foreign
$68.00, one year
$115.00, two years

Schafer AI: Bleeding and thrombosis in the myeloproliferative disorders.
Blood 64:1, 1984

(Above rates apply to libraries)

MurphyS: Polycythemia vera. In Hematology, 4th ed, W1lliams WJ et a1
(Eds). McGraw-H111, New York, 1990, pp 193-202

Students
$40.00, one year
$70.00, two years

MurphyS: Primary thrombocythemia. Ibtd, pp 232-236
Hart RG, Kanter MC: Hematologic disorders and ischemic stroke. Stroke
21:1111,1990

(U.S. and possessions only)

Jabaily Jet al: Neurologic manifestations of essential thrombocythemia.
Ann Intern Med 99:513, 1983

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