Motor dysfunction on the nonhemiplegic side in patients with intracerebral haemorrhage.
This study was undertaken to evaluate the motor dysfunction on the nonhemiplegic side in patients with acute intracerebral haemorrhage (ICH) and correlate these with radiological and motor evoked potentials findings. 28 patients (23 males, 5 females), with CT proven ICH within 10 days of ictus were subjected to clinical evaluation and central motor conduction studies (CMCT) of upper limbs. The patient's age ranged between 28 and 84 years. Motor signs on the nonhemiplegic side were present in 17 patients in the form of increased tone (10), hyperreflexia (13) and extensor plantar response (10). Sixteen of these patients had severe weakness on the hemiplegic side. Most of the patients had putaminal haemorrhage (13) and thalamic and lobar haemorrhage was seen in 2 patients each. The motor dysfunction on the nonhemiplegic side correlated with midline shift but not with the size of haematoma. CMCT findings correlated with motor signs on the nonhemiplegic side in 6 patients. In the patients without any signs on the nonhemiplegic side, CMCT was normal. Out of 17 patients with motor dysfunction on the nonhemiplegic side 9 revealed improvement in CMCT at 1 month followup. The patients with CMCT abnormalities on the nonhemiplegic side either died (2) or had poor outcome (9). Motor dysfunction on the nonhemiplegic side may be due to tentorial herniation and suggests a poor outcome.
Subtle changes in muscle power on the nonhemiplegic side in patients with intracranial lesion including stroke have been reported.,,, In patients with acute stroke, especially with large intracerebral haematoma, the motor signs on the nonhemiplegic side may be due to transtentorial herniation. In an earlier study central motor conduction time (CMCT) abnormalities on the nonhemiplegic side in 12 patients with intracerebral haemorrhage have been reported. The present study aims at evaluating the frequency and pattern of motor signs on nonhemiplegic side and correlate these with CMCT and CT scan findings.
Thirty eight patients with CT proven intracerebral haemorrhage within 10 days of ictus were examined. Ten of these patients were excluded from the study due to history of transient ischaemic attack, stroke and demonstrable CT lesions other than haematoma. All the patients underwent a detailed clinical evaluation. The level of consciousness was assessed by Glasgow coma scale and power by MRC (Medical research council) scale. Tone, reflexes, pupillary asymmetry, hyperventilation and gastric haemorrhage were also recorded. Cranial CT scan was carried out within 12 hours of admission, if not already available. The CT scan was reviewed for size, location, midline shift and ventricular extension of the haematoma. The midline shift exceeding 5 mm was considered abnormal. The haematoma was classified into small, medium and large according to the largest diameter i.e. <2 mm, 24 mm and more than 4 cm respectively. Motor evoked potentials were recorded by stimulating the motor cortex by a high voltage electrical stimulator, Digitimeter DI80, delivering a shock up to 750 V with a time constant of 50-100. To activate abductor digiti minimi (ADM) the cathode was placed at the vertex and anode 7 cm lateral and 1 cm anterior to the line drawn from vertex to the tragus contralateral to recording site. A current of 80-100% of the maximum output was delivered while the patient was asked to contract his ADM slightly (10% of the maximum force) irrespective of the degree of weakness. For cervical stimulation the cathode was placed below the spinous process of the seventh cervical vertebra and the anode proximally giving 50-60% of the maximum output while the subject was asked to relax. The minimum onset latency and the amplitude of the negative phase were recorded. Central motor conduction time (CMCT) was calculated by the difference between the cortical and spinal latencies. The results were compared with the normal values of our laboratory which was obtained from 32 healthy adults whose age ranged between 18 and 50 years. The abnormality was defined as the absence of MEP or significant prolongation of CMCT (mean+2.5 SD of controls). The upper limit of CMCT in our laboratory was 8.1 ms. The clinical signs of motor dysfunctions on the non hemiplegic side were correlated with radiological and CMCT changes employing X2 test.
This study is based on 28 patients with intracerebral haemorrhage. Their age ranged between 28 and 84 years (mean 50.2 years) and 5 of them were females. Three patients were admitted within 24 hours, 10 within 3 days, 8 within 7 and 7 patients within 10 days of ictus.
Clinical signs: Motor signs were present on the nonhemiplegic side in 17 patients which included increased tone in 10, hyperreflexia in 13 and extensor plantar response in 10 patients. Pupillary asymmetry was present in 3, hyperventilation in 1, gastric haemorrhage in 2 and sinus tachycardia was present in 7 patients. Sixteen patients had severe weakness on the hemiplegic side (MRC grade 0-2) and one had partial weakness (MRC grade 3-4). The Glasgow coma scale ranged between 6 and 14 (mean 10.2).
Out of eleven patients who did not have signs of motor dysfunction on the nonhemiplegic side, pupillary asymmetry was seen in one, hyperventilation in 4 and sinus tachycardia in two patients. None of these patients had gastric haemorrhage. In this group the weakness on the hemiplegic side was severe in 5 patients (MRC grade 0-2) and mild in 6 patients (MRC grade III-IV). The Glasgow coma scale ranged between 7 and 13 (mean 10.9).
Radiological findings: The motor dysfunction on the nonhemiplegic side was present most frequently in putaminal haemorrhage (N=13, 78%), followed by thalamic and lobar haemorrhages (2 patients, 12% each). In contrast to this, in the group without motor dysfunction on the nonhemiplegic side the haematoma was thalamic in 6 patients, (54%) and putaminal in 5 patients, (46%). The motor dysfunction on the nonhemiplegic side did not correlate with the size of haematoma (X2=0.09, df=l, NS). Midline shift exceeding 5 mm on CT scan correlated with motor dysfunction on the nonhemiplegic side (X2=3.85, df=l, P<0.05). Nine out of 11 patients with midline shift had motor dysfunction on the nonhemiplegic side. Two patients had intraventricular extension of haematoma and one had uncal herniation. All the three patients had motor dysfunction on the nonhemiplegic side.
Central motor conduction findings: CMCT findings correlated with motor dysfunction on the nonhemiplegic side in 6 patients. These were prolonged in 4 and unrecordable in 2 patients. The GCS score in these patients ranged between 6 and 14 (mean 8.6).
In the patients without motor dysfunction on the nonhemiplegic side, CMCT was normal. In these patients GCS score ranged between 7 and 13 (mean 10.9). The distribution of patients with abnormal CMCT on the nonhemiplegic side included increased tone in 3, hyperreflexia and extensor plantar response in 5 patients each. The haematomas were located in putamen in 4 and in thalamus in 2 patients; the haematoma was large in 4 and medium size in 2 patients. Midline shift was present in 5 out of 6 patients. On the hemiplegic side CMCT was abnormal in 22 patients; unrecordable in 19 and prolonged in 3 patients.
Followup studies: Out of 17 patients with motor dysfunction on the nonhemiplegic side, sequential followup was possible in 11 patients. Two of these patients died. In both these patients, CMCT was unrecordable on the nonhemiplegic side. One patient died in the first week and the other in the second month of illness. In the remaining 9 patients the clinical signs on the nonhemiplegic side improved within first week in 5, and by 4th week in the remaining patients. The CMCT studies at the end of 1 month revealed improvement in 2 out of 3 patients, in whom it was possible. The patient with abnormal CMCT on the nonhemiplegic side either died or had a poor outcome.
In the group without motor dysfunction on the nonhemiplegic side, 5 patients could be followed up. The initial Barthel Index score in these patients improved by one month (mean 3.4, range 5-19).
The motor dysfunction on the nonhemiplegic side correlated with midline shift (X2=3.85, df=l, P<0.05) and severity of weakness on the hemiplegic side (X2=4.08, df=l, P<0.05).
In our study on ICH, clinical signs of motor dysfunction on the nonhemiplegic side were present in 17 out of 28 patients. Of these, CMCT was abnormal in 6 and radiological signs of midline shift were present in 9 patients. The motor dysfunctions on the nonhemiplegic side correlated with the outcome.
The motor dysfunction on the nonhemiplegic side may be due to compression of motor pathways following midline shift and uncal herniation. Medium or large size and rapidity of development of supratentorial haematoma results in herniation. The motor pathways in midbrain, may be compressed against tentorium as a result of tentorial herniation and in an extreme case there may even be infarction of occipital lobe due to compression of posterior cerebral artery although the latter was not found in any of our patients. The compression of midbrain may explain hyperventilation and pupillary asymmetry in some patients.
In 8 patients who did not have midline shift or radiological evidence of herniation, clinical signs of motor dysfunction on the nonhemiplegic side were present. This may be attributed to crossed cerebral diaschiasis. Cross cerebral diaschiasis has been described in stroke patients which may result in transient hypometabolism on the uninvolved side and may be responsible for various neurological dysfunctions on the nonhemiplegic side.
In patients with stroke, the muscle strength ipsilateral to the lesion has been reported to be reduced compared to normal control. Ipsilateral deficits have been reported for more complex motor task.,
The ipsilateral weakness would be expected to result following unilateral lesions if each cerebral hemisphere has bilateral projections and these have been demonstrated in subhuman primates and cranial muscles in humans., If all the arm muscles received equal amount of bilateral input then it might be expected that the weakness of the spared side of the paretic patients would parallel their affected side and that all muscles will be equally weakened on the spared side of the plegic patient. In our patients detailed power testing was not possible because of altered sensorium in most patients. We have relied upon change in tone, reflex and CMCT abnormalities for defining motor dysfunction on the nonhemiplegic side.
Power testing is not very reliable in patients with acute stroke. In our patients, motor dysfunction on the nonhemiplegic side is likely, due to compression or dysfunctions of motor pathway of the uninvolved side, as many of our patients had evidences of midline shift and signs of herniation. In our earlier study we have reported the ipsilateral motor response to be an artifact. In human beings, the importance of ipsilateral motor pathways has been demonstrated in chronic lesions such as cerebral palsy due to intrauterine infections. In acute lesions especially in adults, however, their role needs further evaluation.
Sequential studies revealed that clinical signs and CMCT improved in all the patients at the end of one month, which correlated with the clinical improvement in most patients, which again support the role of uncal herniation and midline shift in the genesis of motor dysfunction on the nonhemiplegic side. The role of cerebral diaschiasis however can not be definitely evaluated in our patients and needs further studies employing SPECT or PET Study.