Isolated Hand Weakness in Cortical Infarctions

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1 BRIEF COMMUNICATION Isolated Hand Weakness in Cortical Infarctions Po-Lin Chen, 1 Hung-Yi Hsu, 1,2 Pao-Yu Wang 1,2 * Isolated hand weakness due to stroke is infrequently observed, and often misdiagnosed as peripheral lesions. This study investigated the clinical and radiologic profiles in such patients. Five men and one woman were studied. All patients underwent cranial magnetic resonance imaging (MRI) to confirm the di- agnosis. Four patients had uniform weakness and the other two had either differential radial or ulnar weakness, respectively. MRI showed acute infarctions involving the hand knob area of the primary motor cortex (M1) in five patients and the postcentral gyrus sparing the precentral gyrus in one patient. Two patients with uniform digit weakness had additional involvement of the inferior parietal lobule. These findings suggest that isolated or predominant hand weakness in patients with cerebral infarctions is not necessarily caused by lesions in the M1 knob area, and that the control center of hand movement is not limited to the knob area alone. [J Formos Med Assoc 2006;105(10): ] Key Words: cortical infarctions, hand weakness, primary motor cortex Isolated hand weakness can result from central or peripheral neurologic diseases. The etiology of pure motor hand weakness due to peripheral neurologic diseases encompasses amyotrophic lateral sclerosis, multifocal motor neuropathy with persistent conduction block, juvenile segmental spinal muscular atrophy, cervical radiculopathy, thoracic outlet syndrome, neuralgic amyotrophy, anterior and posterior interosseous neuropathy, compression of the recurrent motor branch of the median nerve, distal ulnar compression at the canal of Guyon, myasthenia gravis, myotonic muscular dystrophy, inclusion body myositis and distal myopathy. 1 Isolated hand weakness due to stroke is infrequently observed, 2 4 and may simulate median or ulnar neuropathy. 5,6 The organization of the primary motor cortex (M1) has been studied widely since Penfield and Boldrey 7 first published their work on the homuncular organization of motor cortex in man in The presence of somatotopic gradients, in which thumb and index finger movements are slightly more heavily represented laterally and little and ring finger movements are slightly more heavily represented medially, is seen either by clinical evidence or magnetic resonance imaging (MRI) studies. 2,5 The aim of this work was to establish the clinical and radiologic profiles in such patients with cortical infarctions. Methods Six patients with hand palsy between December 1991 and June 2003 were included in this retro- spective study, all of whom met the following inclusion criteria: a motor deficit of the fingers with 2006 Elsevier & Formosan Medical Association Division of Neurology, Department of Internal Medicine, Taichung Veterans General Hospital, and 2 National Yang-Ming University School of Medicine, Taipei, Taiwan. Received: January 28, 2005 Revised: July 11, 2005 Accepted: November 1, 2005 *Correspondence to: Dr Pao-Yu Wang, Division of Neurology, Department of Internal Medicine, Taichung Veterans General Hospital, 160, Section 3, Taichung-Kang Road, Taichung 407, Taiwan. pywang@vghtc.gov.tw J Formos Med Assoc 2006 Vol 105 No

2 P.L. Chen, et al or without motor deficit of the wrist and shoulder while the face and lower extremities were spared; motor deficit due to clinically and radiologicallyconfirmed cerebral cortical lesions. Patients who initially presented with a motor deficit in hemiparesis, but subsequently improved to a monoplegia of upper extremity or limited hand palsy, were excluded. All patients were fully examined by at least two neurologists. The medical histories and risk factors were recorded. Data on risk factors for ischemic strokes were obtained for each patient and included the following: a history of hypertension, angina pectoris, hyperlipidemia, diabetes and cigarette smoking. Cranial MRI was performed in all patients. T1-weighted images (T1WI), T2-weighted images (T2WI) and fluidattenuated inversion recovery images were obtained for each patient. Four patients also underwent magnetic resonance angiography (MRA). The infarction and the vascular territory were localized by MRI according to the atlas of Jurgen et al. 8 Data from other diagnostic procedures, including electrocardiography, transcranial color-coded sonography and duplex of neck were analyzed. Electromyography (EMG) and nerve conduction study (NCS) were performed in one patient with sensory deficits. Electroencephalography was performed in one patient with a seizure attack. Sub- types of cerebral infarction were classified using the Trial of ORG in Acute Stroke Treatment (TOAST) criteria. 9 Results Six patients with cerebral infarctions were included. The clinical profiles of these patients are summarized in the Table. The motor deficit was always primary and could be distinguished from motor neglect, ataxia and apraxia. Four patients had at least one of the following risk factors: atrial fibrillation (one patient), hypertension (three patients), hypercholesterolemia (one patient) and cigarette smoking (one patient). Four patients had uniform involvement of all digits, one patientt had differential radial weakness involving the Table. Clinical data and anatomical localizations of lesions in patients with isolated hand weakness after cortical infarction Patient Age (yr) Gender M M M M F M Course of onset A A SA A A A Side of hand weakness R L R R R L Weakness of digits UF UF RW UF UF UW Proximal arm weakness + Sensory impairment + Deep tendon reflexes N N N N N N Babinski s sign F F F F E F Subtype of IS CE AS U U U AS Anatomical localizations Precentral gyrus Postcentral gyrus + Inferior parietal lobule +, AG +, AG Corona radiata + Other MFG M = male; F = female; A = acute; SA = subacute; R = right; L = left; UF = uniform weakness; RW = radial weakness; UW = ulnar weakness; = absent; + = present; N = normal; F = flexor type; E = extensor type; IS = ischemic stroke; CE = cardioembolic; AS = atherosclerotic; U = undetermined; AG = angular gyrus; MFG = middle frontal gyrus. 862 J Formos Med Assoc 2006 Vol 105 No 10

3 Hand weakness in cortical infarctions thumb and index, and one had differential ulnar weakness involving the third to fifth fingers. One patient had moderate weakness of the wrist and mild weakness of the elbow and shoulder, but the face and lower extremities were spared. The motor deficit started acutely in five patients and subacutely in one. The patient with a subacute onset of motor deficit (patient 3) had weak flexion of the thumb at first, and then the index in 1 week. Both headache and simple partial clonic seizure occurred in patient 5. Deep tendon reflexes were normal in all cases. Babinski s sign was of flexor type in all patients except patient 5. None of the patients with uniform digit weakness had sensory dysfunction. In addition to radial weakness, patient 3 had sensory deficits of pin-prick and light touch of thumb and index. None of the patients had impairment of object recognition in the weak hand, or exhibited aphasia or hemianopsia. The anatomic localizations of the lesions identified on MRI are shown in Figure 1 and listed in the Table. Four patients had infarctions in the left hemisphere, and two had infarctions in the right hemisphere. The M1 knob area was involved in five patients. Patient 3 had infarction at the left postcentral gyrus instead of the precentral gyrus (Figure 2A). The cranial MRI of patient 5 is shown in Figure 2B. Both of the patients with uniform hand weakness (patients 1 and 2) had infarctions involving left angular gyri in addition to the M1 knob areas. Four patients (patients 1, 3, 4, 5) had normal findings on cerebral vascular ultrasound and MRA. MRA showed severe stenosis of the left vertebral artery and right middle cerebral artery (MCA) in patient 2 and moderate stenosis of the right MCA in patient 6. Cardiac work-ups showed atrial fibrillation in patient 1, but no potential cardiac sources of embolisms were found in the other patients. One patient whose neurologic deficits simulated median neuropathy (patient 3) had normal EMG/NCS studies, while another who had seizure attack at the onset (patient 5) had a normal electroencephalogram. Both of these patients had normal findings on surveys of possible underlying connective tissue diseases or hypercoagulable diseases including anticardiolipid antibodies, antinuclear antibodies, protein C, protein S, fibrinogen and homocystein in blood. The infarctions were classified as cardioemc bolic in one patient, large-artery atherosclerotic in two and of undetermined etiology in three. Among four patients with uniform digit weakness, three had full recovery of hand palsy, and one (patient 5) had Medical Research Council digit muscle power of grade 4 at 3 months. Two patients with differential weakness had complete recovery. Discussion In this study, two patients had differential weakness in the radial and ulnar distributions, respectively. Isolated hand weakness by cerebral infarction can cause uniform hand weakness, or differential Figure 1. Lesion reconstructions from axial magnetic resonance imaging in patients with cerebral infarction. Each vertical column of sections represents a single patient. Left and right sides are reversed. The sections are at a 0 angle. J Formos Med Assoc 2006 Vol 105 No

P.L. Chen, et al A B Figure 2. Cranial magnetic resonance imaging (MRI).

T1WI with contrast, respectively, from left to right.

weakness in either radial (thumb and index) or ulnar digits (little and ring fingers).

3 Two patients who had uniform digit weakness in this series (patients 1 and 2) had infarctions at the contralateral angular gyri in addition to the M1 knob area.

A positron emission tomography study also showed that the inferior parietal lobule was activated during imaginary hand grasping.

11 Although patients with ischemic stroke may have no or minor paresis, they may have motor deficits concerning force control, fine movements and manipulation with the hand contralateral to the

4 P.L. Chen, et al A B Figure 2. Cranial magnetic resonance imaging (MRI). (A) Cranial MRI of patient 3 shows an infarction (arrows) at the left postcentral gyrus with spared precentral gyrus on T1-weighted image (T1WI), fluid-attenuated inversion recovery image (FLAIR) and T1WI with contrast, respectively, from left to right. (B) Cranial MRI of patient 5 shows a small infarction (arrows) in the knob area of the left primary motor cortex on T1WI, FLAIR and T2-weighted images, respectively, from left to right. weakness in either radial (thumb and index) or ulnar digits (little and ring fingers). 2,4,5 Our literature review found no previous report of selective weakness of a single digit other than the thumb due to ischemic stroke. 3 Two patients who had uniform digit weakness in this series (patients 1 and 2) had infarctions at the contralateral angular gyri in addition to the M1 knob area. Finger agnosia and agraphia, which are well known deficits of the Gerstmann syndrome, illustrate that the angular gyrus is crucial in controlling hand movements. A positron emission tomography study also showed that the inferior parietal lobule was activated during imaginary hand grasping. 10 The inferior parietal lobule, especially angular gyrus, is important in controlling hand movement by visuomotor transformation. 11 Although patients with ischemic stroke may have no or minor paresis, they may have motor deficits concerning force control, fine movements and manipulation with the hand contralateral to the lesion. Timsit et al 4 reported three patients with isolated hand palsy who had contralateral angular gyri infarctions that completely spared the pyramidal tract. In the present study, patients 1 and 2 had hand weakness but not apraxia, and it is possible that the pathology in the involved inferior parietal lobule might have had a superimposed effect on the hand weakness. One patient in this series (patient 3) also had a small nonpyramidal infarction located at the left postcentral gyrus. The pathogenesis by which sensory deficits result in motor deficits may be explained by the occurrence of sensorimotor transformation as reported by Pause and Freund 12 and corticocortical connections between somatosensory cortex, parietal lobe and primary motor cortex. 13 These authors reported that patients with more posteriorly located parietal lesions had predominantly severe disturbances of complex sensibility, precision grip, manipulation and explorative finger movements. 12 The above studies 4,10 13 suggest that sensory integration may synchronize the activities between spatially distributed cortical sites. Any insult involving the network of hand control might result in hand apraxia or weakness. 864 J Formos Med Assoc 2006 Vol 105 No 10

5 Hand weakness in cortical infarctions Isolated hand weakness caused by central lesions is most commonly caused by embolic strokes involving the M1 knob area, 3,5 but large-artery atherosclerotic infarctions also play a significant role. Timsit et al 4 reported that the pathogenesis of infarctions at the angular gyri was hemodynamic compromise with stenosis of ipsilateral internal carotid artery. In the present series, two of six patients had a diagnosis of atherosclerotic infarction, and one had cardioembolic infarction. Isolated hand palsy caused by lacunar infarctions in subcortical areas is relatively uncommon. 6 This study also found that most patients with isolated hand weakness of ischemic infarctions have good recovery. The good recovery may be closely related to the reorganization of M1 after insult, 14 and may be associated with the adjacent cortical areas taking over the function of the damaged areas or utilization of alternative motor pathways. 15 It is important to differentiate central from peripheral lesions because of the requirement for different treatment modalities. Some of the clinical clues which may help differentiate central from peripheral lesions include muscles affected in groups, absence of atrophy and fasciculation, presence of spasticity, hyperactivity of deep tendon reflexes and extensor plantar reflexes. However, weakness pattern of central lesions at the M1 knob may simulate median or ulnar neuropathy. 5,6 Deep tendon and plantar reflexes could be normal as demonstrated in this study and several previous studies. 2,4,6 NCS and EMG are helpful when clinical clues are not conclusive. In conclusion, this study suggests that isolated or predominant hand weakness in cerebral infarctions is not necessarily caused by lesions in the M1 knob area, and the control center of hand movement is not limited to the knob area alone. Detailed neurologic examination is necessary to understand the role of the cortical networks in controlling pathologic hand motor movement after ischemic stroke. Such examination must include every single digit, and correlate with the anatomic locations by imaging studies. References 1. Lewis RA. Pure motor hand weakness. Semin Neurol 1996;16: Schieber MH. Somatotopic gradients in the distributed organization of the human primary motor cortex hand area: evidence from small infarcts. Exp Brain Res 1999; 128: Terao Y, Hayashi H, Kanda T, et al. Discrete cortical infarction with prominent impairment of thumb flexion. Stroke 1993;24: Timsit S, Logak M, Manai R, et al. Evolving isolated hand palsy: a parietal lobe syndrome associated with carotid artery disease. Brain 1997;120: Gass A, Szabo K, Behrens S, et al. A diffusion-weighted MRI study of acute ischemic distal arm paresis. Neurology 2001;57: Lampl Y, Gilad R, Eshel Y, et al. Strokes mimicking peripheral nerve lesions. Clin Neurol Neurosurg 1995;97: Penfield W, Boldrey E. Somatic motor and sensory representation in the cerebral cortex of man as studied by electrical stimulation. Brain 1937;60: Jurgen KM, Assheuer J, Paxinos G. Atlas of the Human Brain. San Diego: Academic Press, Adams HP Jr, Bendixen BH, Kappelle LJ, et al. Classification of subtype of acute ischemic stroke. Definitions for use in a multicenter clinical trial. TOAST. Trial of Org in Acute Stroke Treatment. Stroke 1993;24: Decety J, Perani D, Jeannerod M, et al. Mapping motor representations with positron emission tomography. Nature 1994;371: Jeannerod M, Arbib MA, Rizzolatti G, et al. Grasping objects: the cortical mechanisms of visuomotor transformation. Trends Neurosci 1995;18: Pause M, Freund HJ. Role of the parietal cortex for sensorimotor transformation. Evidence from clinical observations. Brain Behav Evol 1989;33: Lewis JW, van Essen DC. Corticocortical connections of visual, sensorimotor, and multimodal processing areas in the parietal lobe of the macaque monkey. J Comp Neurol 2000;428: Duffau H. Acute functional reorganisation of the human motor cortex during resection of central lesions: a study using intraoperative brain mapping. J Neurol Neurosurg Psychiatry 2001;70: Chen R, Cohen LG, Hallett M. Nervous system reorganization following injury. Neuroscience 2002;111: J Formos Med Assoc 2006 Vol 105 No

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Title. CitationInternal Medicine, 46(8): Issue Date Doc URL. Type. File Information Title Scapular Winging as a Symptom of Cervical Flexion My Author(s)Yaguchi, Hiroaki; Takahashi, Ikuko; Tashiro, Jun; Ts CitationInternal Medicine, 46(8): 511-514 Issue Date 2007-04-17 Doc URL http://hdl.handle.net/2115/20467