Pure Motor Hemiplegia Due To Pyramidal Infarction Sudhansu Chokroverty, MBBS, MRCP; Frank A. Rubino, MD; Carol Haller, MD
\s=b\ A 77-year-old man suddenly developed left hemiplegia without sensory impairment, visual or speech difficulties, loss of consciousness, or ataxia. He died one month later of pulmonary embolism, and a cystic infarction in the right medullary pyramid was the only lesion in the corticospinal system. (Arch Neurol 32:647-648, 1975)
that it
and Curry1 stated doubtful that pyramidal Fisher infarct was
a
would result in a pure motor hemiplegia without other medullary signs. However, they mentioned that "a critically placed small lacunar le¬ sion could conceivably be limited to one pyramid, but this has never been reported." To our knowledge, we pro¬ vide the first such anatomically
proved
case.
REPORT OF A CASE A 77-year-old man developed weakness of the left side of his body on Feb 23,1973. In the course of the next 12 to 24 hours, the weakness progressed to a complete pafor publication April 9, 1975. From the Neurology Service and Pathology Section, Veterans Administration Hospital, Hines, Ill; the University of Health Sciences/the Chicago Medical School, Chicago; and Loyola
Accepted
University Stritch School of Medicine, Maywood, Ill.
Reprint requests to PO Box 127, Hines, Il (Dr. Chokroverty).
60141
ralysis.
He did not have
convulsions, im¬
pairment of consciousness, paresthesia, vertigo, diplopia, or visual or speech diffi¬ culties. Past history included sudden onset of monoparesis at the age of 50 years, in¬ volving the right upper extremity with re¬ covery. There was no history of hyperten¬ sion. At the time of admission, the patient's blood pressure was 130/80 mm Hg and his heart rate was 80 beats per minute. On neurological examination, he was fully awake, alert, oriented, and his mental functions were appropriate for his age. He did not have dysarthria or dysphasia. The visual fields were intact, and the pupils were equal. The extraocular were full without nystagmus. Facial sensation was normal. According to one observer, there was a very mild left central facial paresis, while a second ex¬ aminer noted that the face was symmetri¬ cal. There was no palatal or lingual paresis. The patient had a dense left hemiplegia with only a trace of movement in the leg. There was flaccidity in the hémiplégie limbs, but the muscle stretch reflexes were greater in the affected than in the unaf¬ fected side. Plantar response was extensor on the left but flexor on the right side. There was no cerebellar ataxia of the right limbs. There was no sensory deficit to pinprick, touch, vibration, and joint posi¬ tion sense. Two-point discrimination, stereognosis, and right-left orientation were normal. Laboratory data were not singu¬ larly abnormal or indicative of systemic disease. The patient's condition initially im¬ proved. One month after the onset of
movements
Downloaded From: http://archneur.jamanetwork.com/ by a University of Pittsburgh User on 06/20/2015
hemiplegia,
he was able to move his left foot and left fingers against gravity and he could walk a few steps. Changes in muscle tone and stretch reflexes were not documented. On March 27, 1973, his condi¬ tion suddenly deteriorated and he died on March 28. Postmortem findings consisted of pulmo¬ nary infarct in the right lower lobe, cardiomegaly with left ventricular hypertrophy, and severe coronary and moderate gener¬ alized arteriosclerosis. The cerebral hemi¬ spheres were symmetrical but atrophie. Atheromatous plaques were scattered throughout the major cerebral arteries. Se¬ rial coronal sections of the cerebral and cerebellar hemispheres and sections through the mesencephalon, diencephalon, and pons revealed no gross lesions. Trans¬ verse sections of medulla disclosed an area of softening and discoloration in the right
medullary pyramid (Figure). Microscopic
sections of the medulla revealed cystic in¬ farction involving the right medullary pyramid within which were many macro¬ phages and reactive astrocytes. The in¬ farction extended down to just above the level of pyramidal decussation. Demyelination and swelling of the myelin sheaths and axis cylinders were noted in the sur¬ rounding tissues. The margin of the in¬ farction involved portions of inferior olive and medullary tegmentum, including the lateralmost part of medial lemniscus on the right side. A section through the cere¬ bellum showed a focal cystic infarct involv¬ ing part of the dentate nucleus and small healed gliotic infarcts scattered in the cerebellar folia. Sections of cerebral cor-
patients, which included nine autopsies, Fisher and Curry1 concluded that pure motor hemiplegia resulted from a small in¬ farction in the internal capsule or the basis pontis, probably due to throm¬ bosis of the small penetrating vessels. Our patient differed in that a medul¬ lary pyramidal infarct gave rise to pure motor hemiplegia. Although the infarction was not limited to the pyramid, the changes beyond the pyramid were minor, and were not sufficient to cause medullary tegmental dysfunction or signs of cerebellar dysfunction. Weintraub and Glaser2 described a case of pure motor hemi¬ plegia due to a nocardial abscess in the motor cortex, and Igapashi et al3 described a case resulting from is¬ chemia or edema in the motor cortex after recraniotomy for postoperative not involved. In 50
Transverse section of medulla.
magnification
5).
Pyramidal infarction
tex, mesencephalon, diencephalon, basal ganglia, and pons disclosed no histological changes in the corticospinal system and other structures.
COMMENT Fisher and Curry1 defined pure mo¬ tor hemiplegia as a complete or in-
on
right
side
(Myelin, original
complete recent paralysis of the face, arm, and leg on one side, unaccompa¬ nied by any impairment of functions of language, sensory system, visual fields, cerebellar pathways, and cra¬ nial
nerves.
The clinical features in
patient were consistent with this definition, except that the face was
our
Joint Electroencephalography Meet¬ ing.—The American EEG Society, the
Mexican EEG Society, and the Amer¬ ican Society of EEG Technologists will hold a joint meeting Oct 15 through 19,1975, at the Hotel Camino Real, Mexico City. Scientific sessions include free communications and symposia on "Myoclonus and Myo¬ clonic Epilepsy" and "Multiple Unit Activity Recordings in Epilepsy." Courses will be offered in clinical elec¬ troencephalography and fundamental and advanced EEG technology. Spe¬ cial air fare and hotel arrangements are available. For brochure write or
bleeding.
References 1. Fisher CM, Curry HB: Pure motor hemiplegia of vascular origin. Arch Neurol 13:30-44,
1965. 2. Weintraub MI, Glaser GH: Nocardial brain abscess and pure motor hemiplegia. NY State J Med 70:2717-2721, 1970. 3. Igapashi S, Mori K, Ishijma Y: Pure motor hemiplegia after recraniotomy for post-operative bleeding. Arch Jap Chir 41:32-37, 1972.
call the American EEG Society, Exec¬ utive Office, 4137 Erie St, Willoughby, OH 44094. Election of Officers of American Electroencephalographic Asso¬ ciation.—At a recent meeting of the American Medical Electroenceph¬ Medical
alographic Association, the following were elected: president, Rob¬ ert P. Jeub, MD, Minneapolis; presi¬ dent-elect, Thomas J. Holbrook, MD, Huntington, WVa; and secretarytreasurer, Wayland A. Stephenson, officers
MD, Santa Barbara, Calif.
Downloaded From: http://archneur.jamanetwork.com/ by a University of Pittsburgh User on 06/20/2015
\s=b\ A 77-year-old man suddenly developed left hemiplegia without sensory impairment, visual or speech difficulties, loss of consciousness, or ataxia. He died one month later of pulmonary embolism, and a cystic infarction in the right medullary pyramid was the only lesion in the corticospinal system. (Arch Neurol 32:647-648, 1975)
that it
and Curry1 stated doubtful that pyramidal Fisher infarct was
a
would result in a pure motor hemiplegia without other medullary signs. However, they mentioned that "a critically placed small lacunar le¬ sion could conceivably be limited to one pyramid, but this has never been reported." To our knowledge, we pro¬ vide the first such anatomically
proved
case.
REPORT OF A CASE A 77-year-old man developed weakness of the left side of his body on Feb 23,1973. In the course of the next 12 to 24 hours, the weakness progressed to a complete pafor publication April 9, 1975. From the Neurology Service and Pathology Section, Veterans Administration Hospital, Hines, Ill; the University of Health Sciences/the Chicago Medical School, Chicago; and Loyola
Accepted
University Stritch School of Medicine, Maywood, Ill.
Reprint requests to PO Box 127, Hines, Il (Dr. Chokroverty).
60141
ralysis.
He did not have
convulsions, im¬
pairment of consciousness, paresthesia, vertigo, diplopia, or visual or speech diffi¬ culties. Past history included sudden onset of monoparesis at the age of 50 years, in¬ volving the right upper extremity with re¬ covery. There was no history of hyperten¬ sion. At the time of admission, the patient's blood pressure was 130/80 mm Hg and his heart rate was 80 beats per minute. On neurological examination, he was fully awake, alert, oriented, and his mental functions were appropriate for his age. He did not have dysarthria or dysphasia. The visual fields were intact, and the pupils were equal. The extraocular were full without nystagmus. Facial sensation was normal. According to one observer, there was a very mild left central facial paresis, while a second ex¬ aminer noted that the face was symmetri¬ cal. There was no palatal or lingual paresis. The patient had a dense left hemiplegia with only a trace of movement in the leg. There was flaccidity in the hémiplégie limbs, but the muscle stretch reflexes were greater in the affected than in the unaf¬ fected side. Plantar response was extensor on the left but flexor on the right side. There was no cerebellar ataxia of the right limbs. There was no sensory deficit to pinprick, touch, vibration, and joint posi¬ tion sense. Two-point discrimination, stereognosis, and right-left orientation were normal. Laboratory data were not singu¬ larly abnormal or indicative of systemic disease. The patient's condition initially im¬ proved. One month after the onset of
movements
Downloaded From: http://archneur.jamanetwork.com/ by a University of Pittsburgh User on 06/20/2015
hemiplegia,
he was able to move his left foot and left fingers against gravity and he could walk a few steps. Changes in muscle tone and stretch reflexes were not documented. On March 27, 1973, his condi¬ tion suddenly deteriorated and he died on March 28. Postmortem findings consisted of pulmo¬ nary infarct in the right lower lobe, cardiomegaly with left ventricular hypertrophy, and severe coronary and moderate gener¬ alized arteriosclerosis. The cerebral hemi¬ spheres were symmetrical but atrophie. Atheromatous plaques were scattered throughout the major cerebral arteries. Se¬ rial coronal sections of the cerebral and cerebellar hemispheres and sections through the mesencephalon, diencephalon, and pons revealed no gross lesions. Trans¬ verse sections of medulla disclosed an area of softening and discoloration in the right
medullary pyramid (Figure). Microscopic
sections of the medulla revealed cystic in¬ farction involving the right medullary pyramid within which were many macro¬ phages and reactive astrocytes. The in¬ farction extended down to just above the level of pyramidal decussation. Demyelination and swelling of the myelin sheaths and axis cylinders were noted in the sur¬ rounding tissues. The margin of the in¬ farction involved portions of inferior olive and medullary tegmentum, including the lateralmost part of medial lemniscus on the right side. A section through the cere¬ bellum showed a focal cystic infarct involv¬ ing part of the dentate nucleus and small healed gliotic infarcts scattered in the cerebellar folia. Sections of cerebral cor-
patients, which included nine autopsies, Fisher and Curry1 concluded that pure motor hemiplegia resulted from a small in¬ farction in the internal capsule or the basis pontis, probably due to throm¬ bosis of the small penetrating vessels. Our patient differed in that a medul¬ lary pyramidal infarct gave rise to pure motor hemiplegia. Although the infarction was not limited to the pyramid, the changes beyond the pyramid were minor, and were not sufficient to cause medullary tegmental dysfunction or signs of cerebellar dysfunction. Weintraub and Glaser2 described a case of pure motor hemi¬ plegia due to a nocardial abscess in the motor cortex, and Igapashi et al3 described a case resulting from is¬ chemia or edema in the motor cortex after recraniotomy for postoperative not involved. In 50
Transverse section of medulla.
magnification
5).
Pyramidal infarction
tex, mesencephalon, diencephalon, basal ganglia, and pons disclosed no histological changes in the corticospinal system and other structures.
COMMENT Fisher and Curry1 defined pure mo¬ tor hemiplegia as a complete or in-
on
right
side
(Myelin, original
complete recent paralysis of the face, arm, and leg on one side, unaccompa¬ nied by any impairment of functions of language, sensory system, visual fields, cerebellar pathways, and cra¬ nial
nerves.
The clinical features in
patient were consistent with this definition, except that the face was
our
Joint Electroencephalography Meet¬ ing.—The American EEG Society, the
Mexican EEG Society, and the Amer¬ ican Society of EEG Technologists will hold a joint meeting Oct 15 through 19,1975, at the Hotel Camino Real, Mexico City. Scientific sessions include free communications and symposia on "Myoclonus and Myo¬ clonic Epilepsy" and "Multiple Unit Activity Recordings in Epilepsy." Courses will be offered in clinical elec¬ troencephalography and fundamental and advanced EEG technology. Spe¬ cial air fare and hotel arrangements are available. For brochure write or
bleeding.
References 1. Fisher CM, Curry HB: Pure motor hemiplegia of vascular origin. Arch Neurol 13:30-44,
1965. 2. Weintraub MI, Glaser GH: Nocardial brain abscess and pure motor hemiplegia. NY State J Med 70:2717-2721, 1970. 3. Igapashi S, Mori K, Ishijma Y: Pure motor hemiplegia after recraniotomy for post-operative bleeding. Arch Jap Chir 41:32-37, 1972.
call the American EEG Society, Exec¬ utive Office, 4137 Erie St, Willoughby, OH 44094. Election of Officers of American Electroencephalographic Asso¬ ciation.—At a recent meeting of the American Medical Electroenceph¬ Medical
alographic Association, the following were elected: president, Rob¬ ert P. Jeub, MD, Minneapolis; presi¬ dent-elect, Thomas J. Holbrook, MD, Huntington, WVa; and secretarytreasurer, Wayland A. Stephenson, officers
MD, Santa Barbara, Calif.
Downloaded From: http://archneur.jamanetwork.com/ by a University of Pittsburgh User on 06/20/2015
