Severe motor aphasia after reinfusion of cryopreserved autologous stem cells after myeloablative conditioning.

BACKGROUND: Autologous peripheral blood stem cells (PBSCs) are usually cryopreserved before high-dose chemotherapy (HDCT) and autologous peripheral blood stem cell transplantation (PBSCT). The freezing process requires the addition of cryoprotectants such as dimethyl sulfoxide (DMSO), which is vital for cell viability in frozen aliquots. DMSO has a number of well-described side effects. However, severe neurologic side effects assigned to DMSO are exceedingly rare. CASE REPORT: A 64-year-old female underwent HDCT followed by PBSCT as consolidation therapy in relapsed high-grade (Grade 3B) Stage IIIA follicular lymphoma. PBSCs were mobilized using granulocyte-colony stimulating factor and plerixafor after the second cycle of R-DHAP (rituximab, dexamethasone, high-dose Ara-C, cisplatin) salvage chemotherapy. A total of 7.18 × 106 /kg body weight CD34+ cells were cryopreserved using 10% DMSO. HDCT was administered some weeks later followed by reinfusion of two bags of PBSCs, each containing 98 mL with 1.6 × 106 /kg body weight CD34+ cells. Within a few minutes the patient developed a motor aphasia and became very agitated. Brain imaging did not reveal any pathologic finding. After being transferred to the intensive care unit the patient's condition steadily improved and the motor aphasia resolved completely within 6 hours after its onset. CONCLUSION: This is, to our knowledge, the first report to describe an episode of severe motor aphasia during PBSCT. Given the close timely correlation with PBSCT, this episode appears to be caused by dimethyl sulfoxide (DMSO) and might possibly have been prevented by use of lower concentrations of DMSO.

Acute bilateral cerebral infarction in the presence of neuromyelitis optica spectrum disorder: A case report.

RATIONALE: Neuromyelitis optica spectrum disorders (NMOSDs) are inflammatory demyelinating disorders of the central nervous system; they are characterized by severe optic neuritis and transverse myelitis. Intravenous methylprednisolone pulse (IVMP) therapy is an effective treatment that is administered to patients in the acute phase of NMOSD; this therapy has achieved remarkable results in clinical practice. However, there are no reports on NMOSD patients who have experienced an acute bilateral cerebral infarction while undergoing IVMP treatment. PATIENT CONCERNS: We report on a 62-yr-old woman who was undergoing IVMP therapy for the primary diagnosis of NMOSD. Unexpectedly, the patient's existing limb weakness worsened, and she developed motor aphasia on the second day of IVMP treatment. Additionally, brain magnetic resonance imaging revealed acute bilateral cerebral infarction. DIAGNOSIS: The patient's clinical manifestations, medical imaging results, and laboratory test results were taken into consideration; the final diagnosis was acute bilateral cerebral infarction in the presence of NMOSD. INTERVENTIONS: Subsequent to the onset of acute cerebral infarction, the patient was immediately treated with oral aspirin, atorvastatin, and intravenous butylphthalide. The hormone dose was adjusted to an oral 60-mg/d dose for maintenance; this was followed by immunoadsorption plasmapheresis for 3 days, and double-filtration plasmapheresis for 2 days. OUTCOMES: Following treatment onset, the patient's ocular symptoms significantly improved, and her limb muscle strength gradually recovered. Two months after discharge, the patient's husband reported that she was able to walk with the help of others and take care of herself, and that there was no recurrence. LESSONS: Medical professionals must be aware of the possibility of NMOSD patients with cerebrovascular risk factors suffering an acute cerebral infarction while undergoing high-dose IVMP therapy, as this therapy can exacerbate existing problems.

Reversible nonfluent aphasia and left frontal hypoperfusion during topiramate treatment.

We report the case of a patient with complex partial seizures who developed a nonfluent aphasia when topiramate was added to his therapy. This emergent adverse effect appeared to be reversible, as language performance improved after discontinuation of topiramate. Interictal SPECT performed when the patient was aphasic revealed a focal perfusion reduction in the left lateral and mesial frontal cortex, which was no longer evident at a follow-up study after language recovery.

A cocaine-associated quadriplegia and motor aphasia after first use of cocaine.

UNLABELLED: A 31-year-old female who have snorted one "line" of cocaine hydrochloride (approximately 35 mg), for the first time in her life, was admitted to the hospital because of acute onset of right hemiplegia and left hemiparesis evolving into quadriplegia. Motor aphasia, right eye-ball divergent strabismus and right mouth recess lowering were also observed. CONCLUSIONS: A first time mucosal administration of cocaine hydrochloride even in low dose can cause severe neurological complications like quadriplegia and aphasia. Cocaine-associated stroke can be a diagnostic problem in the emergency room. Unconscious patients or those with acute onset of neurological disorders can form a real diagnostic challenge, especially when there is no evidence of previous drug taking.

Intermittent Transient Motor Aphasia Associated with Acute Lithium Toxicity: A Case Report and Brief Review.

BACKGROUND: Lithium is known to cause certain neurological deficits. However, reports of aphasia secondary to lithium toxicity are scant. We report the case of a 70 year old African American woman with a history of schizoaffective disorder and mild dementia who developed transient intermittent aphasia secondary to lithium toxicity. METHODS: Patient was admitted because of agitation, delusional behavior, and pressured speech. Her previous medications included divalproex sodium 500 mg po bid, valproic acid 250 mg po qd, risperidone 3.5 mg po bid, lorazepam 1 mg po bid, amlodipine besylate 5 mg po qd, levothyroxine sodium 25 mcg po qd, gabapentin 300 mg po qd, amantadine HCl 100 mg po bid, and aspirin 81 mg po qd. Since patient's symptoms have not improved, she was started on lithium 300mg po bid and titrated up to 300 mg po bid and 450 mg po qhs over 7-8 days. Her lithium levels ranged from 0.4 mEq/L on 11/11/16 to 1.5 mEq/L on 11/22/16. Patient was observed to have aphasia symptoms intermittently at lithium level of 1.5 mEq/L. CT scan of head and neurology consultations were unremarkable. The Naranjo Adverse Drug Reaction Probability Scale score was 8 in the probable range for an adverse drug reaction. Patient's sodium was also found to be high at 148 mmol/L. RESULTS: Lithium was discontinued and patient rehydrated with intravenous fluids. Patients aphasia resolved completely in 2-3 days. CONCLUSION: Clinicians should be aware of this rarely reported side effect of lithium particularly in patients at risk for volume depletion and closely monitor fluid intake, lithium level, and potential side effects.

Emergence delirium with transient associative agnosia and expressive aphasia reversed by flumazenil in a pediatric patient.

Multiple factors may contribute to the development of emergence delirium in a child. We present the case of a healthy 12-year-old girl who received preoperative midazolam with the desired anxiolytic effect, underwent a brief general anesthetic, and then exhibited postoperative delirium, consisting of a transient associative agnosia and expressive aphasia. Administration of flumazenil led to immediate and lasting resolution of her symptoms. We hypothesize that γ-aminobutyric acid type A receptor-mediated effects, most likely related to an atypical offset of midazolam, are an important subset of emergence delirium that is amenable to pharmacologic therapy with flumazenil.

Intracystic interferon-α treatment leads to neurotoxicity in craniopharyngioma: case report.

Craniopharyngioma is a benign, cystic suprasellar tumor that can be treated with intracystic chemotherapy. Interferon-α (IFN-α) has been gaining popularity as an intracystic treatment for craniopharyngioma because of its efficacy and supposed benign neurotoxicity profile. In this case report the authors describe a patient who, while receiving intracystic IFN-α, suffered a neurological event, which was believed to be related to drug leakage outside the cyst. This is the first report of a focal neurological deficit potentially attributable to intracystic IFN-α therapy, highlighting the fact that IFN-α may have neurotoxic effects on the central nervous system. Given this case and the results of a literature review, the authors suggest that a positive leak test is a relative contraindication to intracystic IFN-α treatment.

Transient expressive (nonfluent) dysphasia after metrizamide myelography.

Four (3.4%) of 117 patients undergoing metrizamide myelography experienced transient expressive dysphasia 7-8 hr after myelography and lasting up to 36 hr. All four patients had lumbar myelograms obtained with 15 ml of 190 mg l/ml (2850 mg l). Metrizamide was injected via lumbar puncture with a 20 gauge spinal needle under fluoroscopic control. Neurologic complications after metrizamide have been reported, but so far have appeared to be transient. It is likely that the transient expressive dysphasia experienced by the four patients reported here was a neurotoxic reaction, rather than a seizure phenomenon.

Acute methotrexate neurotoxicity: findings on diffusion-weighted imaging and correlation with clinical outcome.

BACKGROUND AND PURPOSE: Acute lymphocytic leukemia (ALL) is a common malignancy of childhood treated with methotrexate (MTX), which is associated with acute neurotoxicity. We evaluated diffusion-weighted (DW) and conventional MR images in children with ALL and acute MTX-induced neurotoxicity, with clinical correlation. METHODS: Five patients aged 12-15 years underwent fluid-attenuated inversion recovery (FLAIR), T2-weighted fast spin-echo and gradient-echo, T1-weighted gadolinium-enhanced spin-echo, and DW imaging within 24 hours of symptom onset. Records were reviewed for the temporal relationship to MTX administration, strokelike symptoms, and neurologic outcome. RESULTS: Six strokelike events were temporally related to intrathecal MTX given 6-11 days before symptom onset. FLAIR images showed abnormal hyperintensity in the callosal splenium in one patient but were otherwise normal. Diffusion abnormalities were frontoparietal in three events and frontal in one; nonfluent aphasia was seen in all. Bilateral frontoparietal diffusion abnormalities were associated with bilateral upper-extremity weakness, right-sided hemiparesis, or left-sided hemiparesis (one patient each); one patient had mild facial droop. Unilateral precentral subcortical diffusion abnormality was associated with contralateral motor deficit and ipsilateral upper-extremity sensory loss. Strokelike symptoms resolved rapidly and were not associated with other signs of encephalopathy. Subsequent intrathecal MTX administration was not associated with recurrence in four patients. CONCLUSION: Diffusion abnormalities in acute MTX neurotoxicity indicated cerebral dysfunction but not necessarily overt structural injury to the cerebrum. Subsequent demyelination or gliosis could not be predicted on the basis of diffusion abnormalities. A single strokelike episode with diffusion abnormalities should not necessarily prompt modification of potentially curative chemotherapeutic regimens.

Chronic colchicine-induced myopathy and neuropathy.

The presented case concerns a 77-year old man who had been chronically taking colchicine for treatment of gout. He was admitted because of a transient ischemic cerebrovascular attack with motor aphasia and complained of preexisting paraesthesias in the lower extremities. Neurological examination revealed a global muscular weakness, absent myotatic reflexes and a diminished sensation. Serum creatine kinase (CK) levels were increased and electromyography showed spontaneous fibrillations in deltoid muscles, positive spikewaves in deltoids and anterior tibial muscles. Motor and sensory conduction velocities were mildly reduced. Nerve biopsy findings were compatible with a chronic axonal neuropathy having produced a significant loss of myelinated axons and also denervation features of unmyelinated axons. In muscle, combined neurogenic and myogenic features were found. The former result from the axonal neuropathy. The latter were mainly characterized by focal myofibrillar disorganisation and accumulation of autophagic vacuoles in muscle fibres. The presented neuromuscular symptoms and signs, the increased CK values, the electromyographic and nerve conduction velocity findings as well as nerve and muscle biopsy observations, are consistent with the diagnosis of colchicine-induced myopathy and neuropathy. Furthermore, the disappearance of paraesthesias, normalisation of CK values, and disappearance of fibrillations and positive spike waves in deltoid and anterior tibial muscles on electromyography, after stopping of the colchicine therapy, supported the diagnosis.

Aphasia, apraxia and neurogenic stuttering as complications of metrizamide myelography (speech deficits following myelography).

Aphasia following metrizamide myelography has been reported infrequently. During a seven-month period, we examined two patients who developed Broca's aphasia, apraxia of speech, oral-buccal-facial apraxia and neurogenic stuttering after intrathecal metrizamide administration. In each case, focal neurologic deficits were accompanied by clinical, electroencephalographic and radiologic signs of generalized neurologic disease. Serial speech and language evaluations initially revealed severe deficits that were largely resolved by the third day post-myelography. Out-patient follow-up examinations demonstrated persistence of mild speech and language abnormalities in each case. Our findings suggest that metrizamide may cause longlasting neurologic dysfunction.

[A case of multiple cerebrovascular and migraine episodes caused by the use of oral contraceptives]. / Osservazioni su un caso di episodi cerebrovascolari multipli ed emicranici da uso di contraccettivi orali.

The Authors report the case of a 32-years-old woman taking oral contraceptives for twelve years, who developed multi-infarct dementia and motor-sensory signs as a consequence of repeated cerebrovascular episodes associated with migraine-like attacks. Neuroradiological findings suggested vascular pathologic changes. Mechanisms of cerebro-vascular diseases related to oral contraception are discussed, especially emphasizing the possibility of intrinsic vascular lesions caused by exogenous steroid stimulation. Epidemiologic and pathophysiological relationship between migraine, stroke and oral contraception are also pointed out.

PIP: The authors report the case of a 32 year old woman taking oral contraceptives (OCs) for 12 years, who developed multi-infart dementia and motor-sensory signs as a consequence of repeated cerebrovascular episodes associated with migraine-like attacks. Neuroradiological findings suggested vascular pathological changes. Mechanisms of cerebrovascular diseases related to OCs are discussed, especially emphasizing the possibility of intrinsic vascular lesions caused by exogenous steroid stimulation. Epidemiologic and pathophysiological relationships between migraine, stroke, and OCs are also pointed out. (author's)

Severe central nervous system toxicity from high-dose cytarabine: expressive aphasia occurring after the second day of treatment.

A patient with acute erythroleukemia secondary to polycythemia vera was treated iv with high-dose cytarabine at a dose of 3 g/m2 every 12 hours. After the fourth dose, he developed an expressive (Broca's type) aphasia and somnolence, which progressed until after the treatment was stopped at the seventh dose. The somnolence cleared partially during the next 2 weeks but recurred after cytarabine was restarted at a dose of 100 mg/m2 daily for 7 days. The patient died 5 days later of refractory extreme thrombocytopenia and bleeding. The normal spinal fluid obtained during life and the postmortem findings were consistent with previously reported findings with central nervous system toxicity from high-dose cytarabine. Three unusual aspects of this case are early onset of symptoms, expressive aphasia as the dominant manifestation, and exacerbation of symptoms with standard doses (100 mg/m2/day).