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Brainstem auditory evoked potentials in tubercular meningitis and their correlation with radiological findings.
Correspondence Address:
The present study has been undertaken to describe brainstem auditory evoked potential (BAEP) changes in tubercular meningitis (TBM) and correlate these with CT scan and MRI findings. 24 patients with TBM were subjected to clinical evaluation and CT scan or MRI study. Outcome was defined by 3 month Barthel index score (BI) into poor (BI<12) and good (BI>or=12). The mean age of patients was 26.4+/-14.9 (range 10-62) years, 8 of them were females. Sixteen patients were in stage III, 5 in stage II and 3 in stage I meningitis. CT scan revealed hydrocephalus in 16, exudate in 9, infarction in 12 and tuberculoma in 3 patients. Brainstem was involved in 3 patients (2 infarction and 1 granuloma). BAEPs were unrecordable in one patient and abnormal in 15. The absolute latencies and inter peak latency (IPL) however were not significantly affected. The wave V/I amplitude ratio was abnormal on 12 sides. The BAEP abnormalities were not related to the stage of meningitis, level of consciousness, any specific CT or MRI changes or outcome at 3 months.
Tubercular meningitis (TBM) differs from pyogenic and viral meningitis by predominant basal involvement, associated granuloma formation, vasculitis, infarction and hydrocephalus.[1],[2] These associated pathologies may affect the brainstem functions. Brainstem auditory evoked potential (BAEP) studies may provide objective noninvasive documentation of these functions. BAEP studies have been extensively conducted in pyogenic meningitis for monitoring hearing loss.[3],[4],[5],[6] We could not get any report of BAEP changes in TBM in the literature. In the present communication, results of BAEP have been correlated with clinical and radiological findings.
Patients with TBM seen between 1996 and 1998 were included in this study. All the patients underwent a detailed neurological evaluation. Consciousness was assessed by Glasgow coma scale (GCS), muscle power by Medical Research Council scale and muscle tone by Ashworth scale.[7] In comatose patients, oculocephalic reflex was noted. Plain and contrast enhanced cranial CT with 10 mm cuts was done in all cases. Cranial MRI was carried out on 2T scanner operating at 1.5T, (Magnetome SP Siemens, Germany). T1WI, proton density and T2 weighted spin echo sequences were obtained. Presence of hydrocephalus, infarction, exudate and tuberculoma were noted. The diagnosis of TBM was based on clinical, CT scan and CSF criteria.7 The clinical criteria included fever, headache and neck stiffness for more than 2 weeks. The supporting evidences were obtained from CSF cells (0.02x109/L or more, with lymphocytic predominance), proteins (more than 1 gm/L), sterile bacterial and fungal culture and CT scan findings for the presence of hydrocephalus and exudate. Evidence of tuberculosis outside the central nervous system and response to antitubercular therapy were noted. In the CT scan, presence of tuberculoma and infarction were recorded. The diagnostic categories included (i) highly probable: clinical and 3 supportive criteria; (ii) probable: clinical and 2 supportive criteria and (iii) possible: clinical and one supportive criteria.[8] The severity of TB meningitis was graded into stage I : meningitis only, stage II : meningitis and neurological signs and stage Ill : meningitis, neurological signs with altered sensorium.[9] Brainstem auditory evoked potentials (BAEP) : BAEP were recorded with 0.1 ms rarefaction click stimulation delivered monaurally at 95 dB. A uniform stimulus strength was used in all the patients because most of our patients had altered sensorium. The stimuli were delivered at a rate of 10 Hz. 2048 responses were twice averaged with a bandpass filter of 100Hz-3kHz.[10] The latencies of different waves and interpeak latencies (IPL) of I-III, I-V and III-V were measured. The results were compared with control values obtained from 30 healthy volunteers, whose age ranged between 15 and 68 years. The upper limit of normal was defined as mean+2.5 SD of control. The amplitude ratio of wave V/I was also calculated and considered abnormal if it was below 1. The clinical and radiological parameters were correlated with BAEP findings. The recovery was defined on the basis of 3 month Barthel index score (BI) into good (BI>12) or poor (BI< 12).[11]
Twenty four patients of TBM were included in this study. Their mean age was 26.4+14.[9] (range 10-62) years. Eight of them were females. Sixteen patients were in stage Ill, 5 in stage II and 3 in stage I meningitis. Their mean GCS score was 10.8+4.2. Cranial nerves were involved in 12 patients; optic nerve in 5 and partial or complete external ophthalmoplegia in 7 patients. In patients with stage I and II meningitis, bedside hearing tests were normal. Focal weakness was present in 17 patients which included quadriplegia in 10, hemiplegia and paraplegia in 3 each and monoplegia in one patient. Cranial CT scan was carried out in all and MRI in 15 patients. Cranial CT scan revealed exudate in 9, hydrocephalus in 16, infarction in 12 and tuberculoma in 3 patients. The infarctions were located mostly in basal ganglia. Brainstem infarction was present in 2 patients only; crus cerebri was involved in 1 and right pontomedullary region in the other. MRI scan was done in 15 patients and revealed additional findings in 8, which included a midbrain granuloma in 1. The MRI in remaining patients revealed supratentorial abnormalities. Brainstem auditory evoked potentials were unrecordable in one and recordable in 23 patients. These were abnormal in 15 of them. The absolute latency of BAEP waveforms was normal in most patients [Figure - 1] except in 3 sides where wave III latency was prolonged. Interpeak latency of I-III was prolonged in 3 sides. Wave V and III were not recordable in 1 and 3 sides respectively. The group difference between absolute latency of waveforms and IPL between TBM patients and controls was not significant. The mean and SD of various BAEP waveforms and IPLs in TBM patients and controls are shown in [Table I]. The V/I amplitude ratio was abnormal in 12 sides, however, the group differences were not significant (Z=-1.43). BAEP and clinicoradiological correlation : The BAEP abnormalities in 15 patients, did not correlate with stage of meningitis (X2=0.04, df=2 NS) and level of consciousness (X2=0.94, df=2 NS). Out of 3 patients in stage I meningitis, BAEP was abnormal in 2, whereas out of 16 patients with stage III meningitis, it was abnormal in 10 patients. The BAEP abnormalities also did not correlate with 3 month outcome (X2=0.10, df=1 NS). At 3 month followup, 6 patients had good and 14 had poor outcome. CT scan abnormalities also did not significantly correlate with BAEP abnormalities. Hydrocephalus was present in 16 patients, 10 of these patients had abnormal BAEP and 8 of whom had abnormal V/I amplitude ratio. The other abnormalities in the patients with hydrocephalus included abnormal wave II in 1, wave III in 6, wave V in 1, I-Ill IPL in 4, III-V IPL in 2 and I-V IPL in 1 patient. Presence of hydrocephalus, however, did not correlate with BAEP abnormality (X2=0.20, df=1, NS). One patient had lateral pontomedullary infarction in whom wave III and V were unrecordable. The other patient had infarction of midbrain and crus and his wave V/I amplitude ratio was abnormal. The distribution of radiological changes in patients with abnormal BAEP are summarised in [Table II].
In this study, BAEP was abnormal in 16 out of 24 patients with TBM. The abnormalities included reduction of wave V/I amplitude ratio, prolongation of I-III IPL; absence of wave III and V; however, the group difference was not significant. The reduction of wave V/I amplitude ratio was the commonest abnormality, and was present in 11 patients. The amplitude reduction may be due to raised intracranial tension (ICT) which often accompanies TBM. Presence of hydrocephalus in 8 patients with V/I amplitude reduction further supports the possibility of raised ICT, although intracerebral pressure monitoring was not undertaken. Reduction of wave V/I amplitude ratio has also been reported in supratentorial space occupying lesion resulting in upper brain stem compression in cats.[12] It has been shown that mechanical compression of upper brainstem causes interference with brainstem circulation. In our study, 2 patients had brainstem infarction. BAEP was abnormal in both. Wave V/I amplitude ratio reduction was seen in 1 and unrecordable wave Ill and V in the other. BAEP has been reported to be useful in monitoring brainstem ischaemia and impending brainstem stroke respectively in patients presenting with vertigo.[13],[14],[15] The BAEP abnormalities are common in the acute stage compared to recovery period.13 Vasculitis, although common in TBM, may be seen in 20.5-55% patients depending on the method of evaluation,[15],[16] but is reported to be rare in vertebrobasilar territory.[1],[17] The infarctions are usually present in supratentorial perforating vessels affecting basal ganglia, thalamus and internal capsular region. In our study, basal ganglionic and capsular infarctions were present in 10 and brainstem stroke in 2 patients only. Prolongation of wave I-III IPL was noted in 3 patients. It suggests abnormality in proximal part of VIII nerve to pontomedullary junction or lower pons around superior olive or trapezoid bodies.[18] The midbrain granuloma was seen in one of our patients in whom wave III was unrecordable. On analysing the CT scan with prolonged I-III IPL, miliary granuloma, hydrocephalus with thalamic and capsular infarctions and hydrocephalus with supratentorial granuloma was present in one patient each. Presence of basal exudate may also result in I-III IPL prolongation. The diversity of BAEP abnormalities and lack of specific pattern may be due to diversity of pathophysiological mechanisms in TBM e.g. in the same patient hydrocephalus, infarctions, tuberculoma and varying degree of raised intracranial pressure (ICP) may be present in various combination at different stages of meningitis. Most of our patients were in stage III, therefore, the correlation of hearing deficit with BAEP changes was not possible. In bacterial meningitis, BAEP studies have been used to monitor the hearing deficit.[3],[5] From this study, it can be concluded that although BAEP abnormalities are frequent in TBM but are probably nonspecific and mostly in the form of reduced V/I amplitude ratio. Further studies are needed including CSF pressure monitoring to evaluate the role of ICP on BAEP changes and possible reversibility of these changes after manoeuvers reducing ICP in TBM.
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