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Case Report an Acute Cerebellar Syndrome Following High-Dose Chemotherapy and a Blood Cell Autotransplant

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Case Report an Acute Cerebellar Syndrome Following High-Dose Chemotherapy and a Blood Cell Autotransplant Bone Marrow Transplantation, (1997) 20, 87–88 1997 Stockton Press All rights reserved 0268–3369/97 $12.00 Case report An acute cerebellar syndrome following high-dose chemotherapy and a blood cell autotransplant K Barnard and KS Hansen Legacy Good Samaritan Hospital, Northwest BMT Program, Portland, OR, USA Summary: cations included metoprolol 50 mg per day and thyroxine 0.1 mg per day. A woman with high-risk stage III breast cancer Neurological examination revealed coarse nystagmus – developed acute cerebellar syndrome 75 days after high- horizontal on lateral gaze and rotary on upgaze. At times, dose chemotherapy and blood cell transplant (BCT). An large amplitude saccades occurred in all directions of gaze, extensive search for metastatic, vascular, metabolic, resembling opsoclonus. A striking bilateral intention tremor infectious, and paraneoplastic etiologies was negative. and truncal ataxia was present. The patient was unable to We postulate a delayed adverse effect of high-dose sit or stand without assistance; there was no dysarthria or chemotherapy as the etiology. myoclonic jerking. Muscle strength and tone were normal. Keywords: cerebellar syndrome; high-dose chemo- Deep tendon reflexes were 2+ in the arms and knees and therapy; breast cancer 1+ at the ankles. Plantar responses were flexor. Sensory examination was normal. The WBC was 5.4 × 109/l, granulocytes 3.6 × 109/l and platelets 281 × 103/l. Hemoglobin was 10.2 g/dl. Electro- We present a case of an acute cerebellar syndrome in a 51- lytes, BUN, creatinine, glucose, calcium, magnesium, phos- year-old woman 10 weeks after high-dose chemotherapy phate, liver enzymes and albumin were normal. Blood cul- with blood cell autotransplant for stage III breast cancer. tures had no growth. Thyroid studies including TSH, T3 We postulate this syndrome resulted from delayed adverse and Free T4 were normal. Influenza A and B titers were effects of high-dose chemotherapy. ,1:8. Tumor markers for carcinoembryonic antigen and CA15–3 levels were negative. HIV I and II, RPR, HTLV- 1 and hepatitis A, B, C had been negative 2 months pre- Case report viously. CSF was clear and colorless with an opening press- ure of 15 cm H2O. Protein was 52 mg/dl (normal, 15–45 A 51-year-old woman with mitral valve prolapse and prior mg/dl), glucose was normal and there was 1 WBC/mm3 hypothyroidism developed stage III-A breast cancer (T3 N1 and no RBC. There were no organisms on gram stain. There M0). She received three cycles of neoadjuvant chemo- were no cancer cells. Anti-neuronal antibodies, specifically 2 therapy (cyclophosphamide 600 mg/m , doxorubicin 60 anti-Yo and anti-Hu were not detectable in the serum or mg/m2 and 5 fluorouracil (5-FU) 600 mg/m2) followed by cerebrospinal fluid. Anti-Ri antibodies were not detectable a modified radical mastectomy. Ten of 14 axillary lymph in the serum. A chest X-ray, CT scan of the abdomen and nodes were positive. Post-operatively, she received three pelvis, bone scan, and two MRIs of the brain with contrast more similar cycles of chemotherapy. High-dose chemo- taken at 2-week intervals were all normal. 2 therapy consisted of cyclophosphamide (6000 mg/m ), thi- After rehydration, the patient continued to require assist- 2 2 otepa (500 mg/m ) and carboplatin (800 mg/m ) followed ance with sitting and preferred to lie quietly in bed. She by a blood cell autotransplant. was treated symptomatically with clonazepam 2 mg by + On day 75 she presented with a 2-day history of dizzi- mouth twice daily, thiamine 100 mg by mouth once daily ness, shakiness and unsteadiness exacerbated by any move- and tapering glucorticoids. Aggressive physical and occu- ment. She had diplopia and was unable to walk without pational therapy aided the patient’s gradual recovery over assistance. There was no focal weakness, dysphagia, a period of 2 to 3 months. Repeat MRI of the brain 4 sphincter incontinence, dysarthria, hearing impairment, months post transplant was normal. One year later her neur- fevers, vomiting, headache, tobacco, alcohol or illicit drug ologic examination is normal, she is able to do household use, or family history of neurological disorders. Medi- chores and has resumed working and driving a car. Discussion Correspondence: Dr KS Hansen, HealthFirst Medical Group, 265 North Broadway, Portland, OR 97227, USA Autotransplant recipients are exposed to multiple sources Received 10 March 1997; accepted 20 March 1997 of neurologic damage including their cancer, drugs, infec- Cerebellar syndrome following high-dose chemotherapy K Barnard and KS Hansen 88 tions or organ failure. This patient’s ataxia, opsoclonus, Our patient did not receive any of the agents which are vertigo and intention tremor were consistent with a cerebel- generally associated with acute cerebellar toxicity. How- lar process. Opsoclonus is a rare disorder of ocular motility ever, in a prospective trial of 27 patients receiving high- and often associated with myoclonus.1,2 Adults with opso- dose carboplatin, etoposide, cyclophosphamide and auto- colous should be studied for cancer, drug or toxin exposure logous BMT, three patients developed reversible cerebellar and infections.1 dysfunction and had normal cerebral CT scan and CSF fin- Metastasis to the central nervous system is in fact the dings17 very similar to this case. most common cause of cerebellar dysfunction in cancer We believe that this syndrome may have been caused by patients.3 In our patient, laboratory and radiological studies high-dose chemotherapy. exclude metastatic breast cancer (including leptomeningeal metastases), demyelinating disease, CNS infections (including post-influenza cerebritis), vascular disorders (such as ischemic or hemorrhagic stroke), metabolic dis- References orders and alcoholic cerebellar degeneration. The clinical course excludes a slow viral infection as an etiological possibility. Two remaining diagnostic possibilities are a 1 Digre KB. Opsoclonus in adults. Report of three cases and paraneoplastic cerebellar degeneration (PCD) or a delayed review of the literature. Arch Neurol 1986; 43: 1165–1175. chemotherapeutic toxic effect. 2 Moll JWB, Henzen-Logmans SC, Splinter TAW et al. Diag- PCD is the most common central paraneoplastic syn- nostic value of anti-neuronal antibodies for paraneoplastic dis- drome occurring in patients with cancer – usually of the orders of the nervous system. J Neurol Neurosurg Psychiatry 4,5 1990; 53: 940–943. lung or ovary. The clinical presentation is similar to 3 Waterhouse DM, Natale RB, Cody RL. Breast cancer and par- 3 patients with diffuse cerebellar lesions and usually aneoplastic cerebellar degeneration. Cancer 1991; 68: 1835– presents with a subacute progressive course that causes sev- 1841. ere functional decline and often death.6 Less commonly, 4 Anderson NE, Rosenblum MK, Posner JB. Paraneoplastic cer- patients show an indolent course, stabilizing with minimal ebellar degeneration: clinical-immunological correlations. Ann neurological deficits.4 Reports of therapy are anecdotal and Neurol 1988; 24: 559–567. there are no randomized trials.3 A presumptive diagnosis 5 Moll JWB, Vecht ChJ. Immune diagnosis of paraneoplastic can be made if: (1) the patient has cancer and a neurological neurologic disorders. Clin Neurol Neurosurg 1995; 97: 71–81. 6,7 6 Graus F, Delattre JY. Immune modulation of paraneoplastic disorder is not explained by other causes; (2) the patient neurologic disorders. Clin Neurol Neurosurg 1995; 97: 112– has the characteristic anti-Purkinje cell antibodies in the 116. serum or CSF.8 Our patient had none of these features. 7 Posner J. Paraneoplastic syndromes (review). Neurol Clin As for the neurologic complications of bone marrow 1991; 9: 919–937. transplantation (BMT), metabolic encephalopathy second- 8 Posner JB, Dalmau J. Clinical enigmas of paraneoplastic neur- ary to multi-organ failure is the most common.9 Patchell et ologic disorders. Clin Neurol Neurosurg 1995; 97: 61–67. al9,10 found that Aspergillus, followed by HSV encephalitis 9 Patchell RA, White Cl, Clark AW et al. Neurologic compli- cations of BMT. Neurology 1985; 35: 300–306. were the most frequent infections in encephalitis associated 10 Davis DG, Patchell RA. Neurologic complications of bone with BMT. Cerebrovascular disorders are the third most marrow transplantation. Neurol Clin 1988; 6: 377–387. common neurological complication of BMT, and cerebral 11 Patchell RA. Neurological complications of organ transplan- infarcts related to endocarditis are the most common vascu- tation. Ann Neurol 1994; 36: 688–703. lar problem.9,10 Other neurological complications of BMT 12 Snider S, Bashir R, Bierman P. Neurological complications include seizures, leukoencephalopathy and myoclonus.11,12 after high-dose chemotherapy and autologous BMT for Hodg- Late development of encephalopathy has been reported to kins disease. Neurology 1994; 44: 681–684. be as high as 13% in one series of autologous BMT 13 MacDonald DR. Neurologic complications of chemotherapy 12 (review). Neurol Clin 1991; 9: 955–967. patients. Cerebellar syndromes are usually related to 14 Hannigan EV, Green S, Alberts DS et al. Results of a SWOG 10 drugs (see below). phase III trial of carboplatin plus cyclophosphamide versus Neurotoxicity of drugs may result from metabolic cisplatin plus cyclophosphamide in advanced ovarian cancer. encephalopathy, intracranial hemorrhage, infections or a Oncology 1993; 50 (Suppl. 2): 2–9. psychological effect.12 High-dose chemotherapy (single or 15 Van Der Wall E, Nooijen WF, Baars JW et al. High-dose
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