Morphopsia,' and Occipitoparietal Lesions Homonymous Metamorphopsia. the Distrib- Activity' Or Cholinergic Underactivity.23 Main

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Morphopsia,' and Occipitoparietal Lesions Homonymous Metamorphopsia. the Distrib- Activity' Or Cholinergic Underactivity.23 Main Letters to the Editor 421 A tex and its related structures.2-48 However, We studied 10 patients with panic disor- J Neurol Neurosurg Psychiatry: first published as 10.1136/jnnp.61.4.421 on 1 October 1996. Downloaded from others have reported that chiasmatic' or ret- der (mean age 29-5 (range 23-35) years) rosplenial lesions6 7 could elicit this symp- and 10 age matched healthy controls (mean tom. This patient had a common putaminal age 27-5 (range 24-34) years). Controls haemorrhage without involvement of the were recruited from the sleep laboratory parietal and occipital lobes, as confirmed by technicians. Patients satisfied criteria for a cranial CT. The results of the VEPs dis- diagnosis of panic disorder according to closed a lesion in the left visual pathway pos- DSM-IV. Protocol exclusion criteria terior to the optic chiasm. Thus the lesion included: (a) a history of major medical or responsible for his visual symptoms is in the neurological illness; (b) a history of sleep left optic radiation. This is the first report panic attacks; (c) current or past evidence of 0t that such a lesion could cause metamor- affective disorders; (d) use of psychotropic phosia. Based on the above mentioned drugs in the two weeks before the study. All reports and our own patient, we propose subjects underwent a 48 hour ambulatory that any lesion along the visual pathway, from polysomnography (Oxford Medilog 9200). the retina to the occipitoparietal cortex, can The ECG signal was played back from the cause metamorphopsia. Retinal lesions elicit tape and digitised at 128 Hz with 8 bit reso- ipsilateral monocular metamorphopsia, chi- lution using a specific option of the Medilog asmatic lesions give rise to bitemporal meta- system. The R-R intervals were detected by B morphopsia,' and occipitoparietal lesions means of a derivate-threshold algorithm; the cause contralateral homonymous metamor- accuracy of the R wave detection on ECG phopsia.28 This patient with injury in the left tracing was improved by fitting each QRS optic radiation complained of contralateral complex by a second order polynomial func- homonymous metamorphopsia. The distrib- tion. The fiduciary point on the ECG was utional pattem of metamorphopsia seems to taken as the maximum of the fitting correspond to the part of the visual pathway parabola to reduce the error due to the low affected. sampling rate.4 The heart rate variability sig- K SHIGA nal was processed using an autoregressive M MAKINO Y UEDA algorithm.' All the spectral calculations were K NAKAJIMA performed on all the successive 300 second Department ofNeurology, Kyoto Prefectural segments of ECG recordings of the second University ofMedicine, Kyoto, Japan night. The analysed time intervals were cho- sen from: (a) awake state at the beginning of Correspondence to: Dr Kensuke Shiga, Department of Neurology, Kyoto Prefectural the night; (b) stage 2 non-REM sleep; (c) University of Medicine, 465 Kajiicho Hirokoji- stages 3-4 non-REM sleep; (d) REM sleep. Kawaramachi, Kamigyo-ku, Kyoto, Japan. We focused on two regions of interest in the 1 Miller NR, Walsh and Hoyt's clinical neuro- spectrum: (1) the low frequency (LF) com- ophthalmology, 4th ed. Vol I. Baltimore: ponent 0-05 to 0-15 Hz: an increase of the Williams and Wilkins, 1982, 166-7. power in this band is commonly associated 2 Mooney AJ, Carey P, Ryan M, et al. Para- with sympathetic activation; (2) the high Figure 1 (A) Drawing of the referring doctor's sagittal parieto-occipital meningioma with visual hallucinations. Am Jf Ophthalmol 1965; frequency (HF) component 0-2 to 0 4 Hz, face. His left cheek seemed to have been scraped 59:197-205. mainly expression of parasympathetic con- and some ofhis leftfingers were missing. (B) A 3 Nass R, Sinha S, Solomon G. Epileptic facial trol. The following variables were evaluated: drawing ofthe curtain lace. A fold of the lace metamorphopsia. Brain Dev 1985;7:50-2. the R-R mean and the power of seemed to have been transformed into an 4 Young WB, Heros DO, Ehrenberg BL, et al. variance, animal's face and it seemed to flow to the right. Metamorphopsia and palinopsia. Arch Neurol LF and HF components, and the sympatho- 1989;46:820-2. vagal balance (LF/HF ratio). We analysed 5 Bender M, Savitsky N. Micropsia and teleopsia the normalised spectral component (ratio or mass effect in either the occipital or pari- limited to the temporal fields of vision. Arch Ophthalmol 1943;29:904-8. between the power density of each spectral etal lobes (fig 2). In the pattem shift visual component and the total evoked potential (VEP), the latency of the 6 Ebata S, Ogawa M, Tanaka Y, et al. Apparent spectral density reduction in the size of one side of the face minus the power in the band 0-0-05 Hz) as http://jnnp.bmj.com/ P100 during right visual hemifield stimula- associated with a small retrosplenial haemor- rhage. J Neuro Neurosurg Psychiatry 1991;54: better measures of the autonomic activity in tion was 11 2-4 ms, which was moderately respect to the absolute numbers; in this way delayed compared with 98-0 ms, the 68-70. latency 7 Imai N, Nohira 0, Miyata K, et al. A case of it is possible to remove the effects of the recorded during stimulation of the left visual metamorphopsia caused by a very localized large variability in the total power measures hemifield, indicating the involvement of the spotty infarct. Clin Neurol 1995;35:302-5. among the several subjects.' We applied left visual pathway posterior to the optic chi- 8 Cohen L, Gray F, Meyrignac C, et al. Selective deficit of visual size perception. _J Neurol ANOVA to determine the changes within asm. NeurosurgPsychiatry 1994;57:73-8. each group through the different conditions. Many reports have attributed the lesion of Differences between the two groups were metamorphopsia to the occipitoparietal cor- evaluated by unpaired two tailed Student's t on September 25, 2021 by guest. Protected copyright. Cardiac autonomic regulation during test. sleep in panic disorder Concerning sleep architecture, no differ- ence was found in the percentages of all Panic disorder is thought to be associated sleep stages between patients with panic dis- with a dysfunction of the autonomic nervous order and controls (values are mean (SD)): system. Power spectrum analysis has been stage 1 non-REM sleep 4-5 (2) v 3 9 (2 7); used recently to quantify spontaneous vari- stage 2 non-REM sleep 49-8 (6-2) v 51-7 ability in heart heart rate in humans. Some (7 4); stages 3-4 non-REM sleep 20-6 (8) v authors have detected pattems of cardiovas- 18-8 (6-7); REM sleep 25-1 (6-8) v 25-5 cular responsivity in panic disorder that can (3-6). No difference was found in the num- be interpreted in favour of sympathetic over- ber of analysed segments in each sleep stage activity' or cholinergic underactivity.23 between the two groups. These studies were performed during wake- Mean R-R showed, both in patients with fulness and the result may reflect states of panic disorder and controls, a trend towards increased anxiety. During sleep there are an increase in all sleep stages compared with repetitive modifications of the autonomic wakefulness before sleep. No difference was nervous system that are constant and not found in R-R mean and variance between influenced by cognitive factors. In the pre- patients and controls in the various condi- sent study, we used power spectrum analysis tions. The LF component (sympathetic of the heart rate variation during sleep in activity) decreased during sleep with mini- patients with panic disorder to verify a possi- mal values during stages 3-4 non-REM Figure 2 Cranial CT on admission, showing a ble intrinsic defect in the autonomic regula- sleep, whereas the HF component (paras- high density area in the left putamen. tion in this disorder. ympathetic activity) displayed a reciprocal 422 Letters to the Editor Table I Heart rate variability in panic disorder and controls jerks and detailed sensory testing were nor- J Neurol Neurosurg Psychiatry: first published as 10.1136/jnnp.61.4.421 on 1 October 1996. Downloaded from mal. Patients (n = 10) Controls (n = 10) Electromyography showed a full recruit- ment on submaximal effort with polyphasic w: potentials in the examined muscles (right LF (nu) 67-9 (11 1)* 53-2 (7 3) HF (nu) 32-1 (8 1)* 42-7 (4 9) arm and right leg) suggesting a myopathy, LF/HF 2-33 (0 88)* 1-28 (0-21) whereas nerve conduction studies were Stage 2 non-REM sleep: within the normal range. An ECG was nor- LF (nu) 39-9 (13-9) 36-2 (15-5) mal. Lumbar puncture was not performed. HF (nu) 60-1 (15-2) 57.3 (11-2) LF/HF 0-84 (0 63) 0-76 (0 48) Brain CT was normal. There was a moder- Stage 3-4 non-REM sleep: ate rise of creatine kinase and lactate dehy- LF (nu) 26-9 (11 1) 25-9 (8-6) drogenase concentrations. Diabetes mellitus HF (nu) 73-1 (14 6) 66-2 (11-6) LF/HF 0 47 (0 41) 0-46 (0-32) was not present. REM sleep: Quadriceps muscle biopsy showed an LF (nu) 56-3 (12 8) 53 2 (16-6) increased variability in the size of fibres; few HF (nu) 43 7 (8 3) 41 5 (14-2) fibres showed subsarcolemmal accumulation LF/HF 1 53 (0 68) 1 83 (1-26) of mitochondria, without a typical ragged Values are means (SD).
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