hemorrhage was not surgically evacuated. Serial CAT scans documented its resolution over five weeks. Eighteen months later the patient’s neurological status was unimproved. His truncal ataxia was severe, confining him to a wheelchair. Palatal and facial myoclonus were first noted at the 1 %month follow-up examination. The results in our patient are in keeping with other recent reports that occasional patients with cerebellar hemorrhage survive without decompressive surgery. Such cases are exceptional. In addition to the 2 patients reported by Heiman and Satya-Murti, Ott et al[2] noted 9 nonoperated survivors of cerebellar hemorrhage. In both of these series, such survivors appeared to be left with little o r no deficit. In contrast, our patient illustrates that survival after nonsurgically treated cerebellar hemorrhage is not always “benign” in terms of morbidity. Indeed, given the inevitable destruction to cerebellar parenchyma caused by an intrinsic hemorrhage, with secondary ischemia and pressure damage to the brainstem from mass effect, it is surprising that these previously reported nonoperated survivors have had such minimal residua.
References I . Heimdn TD, Satya-Murti S: Benign ccrcbellar hemorrhages. Ann Neurol 3:366-368, 1978 2. Ott KH,Kase CS, Ojernann RG, et al: Cerebellar hemorrhage: diagnosis and treatment. Arch Neurol 31:160-167, 1974
limited in response to light but normal on convergence. He was mildly demented and exhibited cerebellar signs of severe gait ataxia and moderate dysarthria, extremity ataxia, and horizontal nystagmus. A normal electroretinogram documented intact outer retinal function, but his pattern visual evoked responses (VERs) showed severely decreased amplitude and moderately increased latency bilaterally. Laboratory studies, including urine and serum copper levels, lumbar puncture, and CAT scan, were normal. Following cessation of paint sniffing, his neurological symptoms slowly subsided, and at the time of his return to Mexico two months later, his visual acuity had improved to 20/30- in each eye, his color vision was mildly impaired (he missed five HRR color plates with each eye), the pupillary light reactions were brisk, and his optic fundi remained normal. The pattern VERs remained abnormal although the latency was less prolonged. Minimal cerebellar dysfunction persisted. Solvent inhalation is considered the single most serious drug problem in Mexico [4] and has achieved considerable popularity in the United States L2]. This case demonstrates that chronic sniffing of toluene-based paint may cause a largcly reversible optic neuropathy. It is likely that continued exposure could result in permanent optic nerve damage. Peggy S, Gott, PhD, tested the VEKs.
Toluene Optic Neuropathy James R. Keane, M D Cerebellar damage associated with exposure to toluene (methyl benzene) has been discussed in this journal by Boor and Hurtig [I]. Visual function was not detailed in their report, and toluene is not known to affect the optic nerves [ 3 ] . O n e case of reversible bilateral optic neuropathy has been reported after industrial exposure to vinyl benzene, however [ S ] . T h e following patient exhibited severe optic nerve and cerebellar dysfunction following chronic inhalation of metallic paint containing toluene as the principal solvent.
A 20-year-old Mexican man was seen several months following the onset of decreased vision and ataxia. For three years previously, it had been his daily practice to inhale Sinclair copper aerosol spray paint from a solvent-soaked rag. This product contains metallic copper, toluene, and xylene as solvents and isobutane propane and methylenechloride as propellants. No other drugs or chemicals were abused. His vision was reduced to 41200 in each eye, with poor color perception, moderately constricted visual fields, and normal optic fundi. His pupillary reactions were severely From the Department of Neurology, Los Angeles CountyUniversity of Southern California Medical Center, 1200 N Srate S t , LQS Angeles, CA 90033.
390 Annals of Neurobogy
Vol 4 No 4
October 1978
References 1. Boor JW, Hurtig HI: Persistent cerebellar ataxia after exposure
to toluene. Ann Neurol 2:440-442, 1977 2. Cohen S: Abuse of inhalants, Pradhan SN, Dutta SN (cds): Drug Abuse: Clinical and Basic Aspects. St Louis, Mosby, 1977, pp 290-302 3. Grdnr WM: Toxicology of the Eye. Second edition. Springfield, IL, Thomas, 1974, p p 1026-1027 4. New York Times, Apr 9, 1978, p 22 5. Prart Johnson JA: Retrobulbar neuritis following exposure to vinyl benzene (styrene). Can Mcd Assoc J 90:975-977, 1964
References I . Heimdn TD, Satya-Murti S: Benign ccrcbellar hemorrhages. Ann Neurol 3:366-368, 1978 2. Ott KH,Kase CS, Ojernann RG, et al: Cerebellar hemorrhage: diagnosis and treatment. Arch Neurol 31:160-167, 1974
limited in response to light but normal on convergence. He was mildly demented and exhibited cerebellar signs of severe gait ataxia and moderate dysarthria, extremity ataxia, and horizontal nystagmus. A normal electroretinogram documented intact outer retinal function, but his pattern visual evoked responses (VERs) showed severely decreased amplitude and moderately increased latency bilaterally. Laboratory studies, including urine and serum copper levels, lumbar puncture, and CAT scan, were normal. Following cessation of paint sniffing, his neurological symptoms slowly subsided, and at the time of his return to Mexico two months later, his visual acuity had improved to 20/30- in each eye, his color vision was mildly impaired (he missed five HRR color plates with each eye), the pupillary light reactions were brisk, and his optic fundi remained normal. The pattern VERs remained abnormal although the latency was less prolonged. Minimal cerebellar dysfunction persisted. Solvent inhalation is considered the single most serious drug problem in Mexico [4] and has achieved considerable popularity in the United States L2]. This case demonstrates that chronic sniffing of toluene-based paint may cause a largcly reversible optic neuropathy. It is likely that continued exposure could result in permanent optic nerve damage. Peggy S, Gott, PhD, tested the VEKs.
Toluene Optic Neuropathy James R. Keane, M D Cerebellar damage associated with exposure to toluene (methyl benzene) has been discussed in this journal by Boor and Hurtig [I]. Visual function was not detailed in their report, and toluene is not known to affect the optic nerves [ 3 ] . O n e case of reversible bilateral optic neuropathy has been reported after industrial exposure to vinyl benzene, however [ S ] . T h e following patient exhibited severe optic nerve and cerebellar dysfunction following chronic inhalation of metallic paint containing toluene as the principal solvent.
A 20-year-old Mexican man was seen several months following the onset of decreased vision and ataxia. For three years previously, it had been his daily practice to inhale Sinclair copper aerosol spray paint from a solvent-soaked rag. This product contains metallic copper, toluene, and xylene as solvents and isobutane propane and methylenechloride as propellants. No other drugs or chemicals were abused. His vision was reduced to 41200 in each eye, with poor color perception, moderately constricted visual fields, and normal optic fundi. His pupillary reactions were severely From the Department of Neurology, Los Angeles CountyUniversity of Southern California Medical Center, 1200 N Srate S t , LQS Angeles, CA 90033.
390 Annals of Neurobogy
Vol 4 No 4
October 1978
References 1. Boor JW, Hurtig HI: Persistent cerebellar ataxia after exposure
to toluene. Ann Neurol 2:440-442, 1977 2. Cohen S: Abuse of inhalants, Pradhan SN, Dutta SN (cds): Drug Abuse: Clinical and Basic Aspects. St Louis, Mosby, 1977, pp 290-302 3. Grdnr WM: Toxicology of the Eye. Second edition. Springfield, IL, Thomas, 1974, p p 1026-1027 4. New York Times, Apr 9, 1978, p 22 5. Prart Johnson JA: Retrobulbar neuritis following exposure to vinyl benzene (styrene). Can Mcd Assoc J 90:975-977, 1964
