Tiago Teodoro

Biopsy-negative, varicella zoster virus (VZV)-positive giant cell arteritis, zoster, VZV encephalitis and ischemic optic neuropathy, all in one

A 72-year-old man developed clinical features of giant cell arteritis (GCA) and ipsilateral ophthalmic-distribution zoster, followed within 2 weeks by VZV encephalitis and 2 months later by ischemic optic neuropathy. Temporal artery biopsy was histopathologically negative for GCA, but contained VZV antigen and VZV DNA in multiple non-contiguous (skip) areas. The collective clinical and laboratory findings revealed a remarkably close temporal association of zoster, multifocal VZV vasculopathy with temporal artery infection, biopsy-negative VZV-positive GCA and VZV encephalitis.

Symptomatic internal carotid artery thrombosis in acute carbon monoxide intoxication.

Stroke has been rarely associated with carbon monoxide (CO) intoxication. We report a symptomatic internal carotid artery (ICA) thrombosis in a patient with acute CO intoxication.

Recovery after copper-deficiency myeloneuropathy in Wilson's disease.

Wilson’s disease (WD) treatment focuses on removing excess copper from the body and preventing reaccumulation, but there are reports of neuropathy and myeloneuropathy (MN) linked to copper deficiency (CD) induced by excessive depletion [1]. Here we report on a WD patient with MN associated with longstanding CD. The patient is a 36-year-old male diagnosed with WD at 20 years old, having displayed generalized dystonia, bradykinesia and freezing of gait. Clinical stability was achieved with zinc sulphate 150 mg/ day and trientine 500 mg/day. In 2006, he developed low urinary copper (24 h urine copper = 128 lg/24 h, recommended 200–500 lg/24 h; serum copper 6.35 lg/dL) [6], which worsened in the following years. In 2008 he was switched to D-penicillamine 600 mg/day due to drug availability problems. Soon after, he developed a nephrotic syndrome with focal segmental glomerular sclerosis which resolved with corticosteroid therapy and switching back to trientine. In February 2011, he developed subjective numbness of both hands and feet and over the following months worsening of gait with frequent falls. In July 2011 neurological examination revealed de novo algic hypoesthesia of the limbs in a ‘‘glove and stocking’’ pattern, postural and vibratory hypoesthesia of the lower limbs and gait ataxia. Analytical studies revealed low serum and urine copper (serum copper 13.3 lg/dL, urine copper 40.5 lg/24 h), low ceruloplasmin (3.0 mg/dL), normal zinc levels (14.7 lmol/ L) and anemia (Hb 8.2 g/dL). Electromyography with conduction velocities revealed a mixed sensory-motor peripheral neuropathy and spinal MRI showed signs of posterior dorsal cord myelopathy (Fig. 1). Other causes of MN were excluded: both vitamin E and B12 levels were normal, and serological tests for HIV, syphilis and autoantibodies were negative. Therefore, a causal relationship between CD and MN was considered as probable. Trientine (500 mg/day) and zinc sulfate (330 mg/day) were substituted for zinc acetate 100 mg daily, which was progressively reduced and stopped in January 2012, due to persistent CD. Copper deficiency resolved by March 2012 (24 h urinary copper = 97 lg/24 h, recommended B100 lg/24 h for zinc monotherapy) [6]. Parallel improvement of sensorial ataxia allowed recovery of walking capacity without assistance. Spinal MRI showed mild regression of myelopathy signs (Fig. 1). Conduction velocities studies disclosed slight improvement in amplitude of sensory action potentials and conduction velocities (Table 1). At this point, zinc acetate 150 mg/day was reintroduced, and his condition remains stable 1 year after treatment. T. Teodoro (&) D. Neutel P. Lobo I. Conceição M. M. Rosa L. Albuquerque J. J. Ferreira Department of Neurology, Hospital de Santa Maria (CHLN, EPE), Lisbon, Portugal e-mail: tiagoteodoro@gmail.com

Vertebral artery dissection mimicking status migrainosus.

Vertebral artery dissection (VAD) may uncommonly present as isolated headache. More rarely, it simulates classical headache syndromes, including migraine. We report a VAD mimicking status migrainosus.

Spinal cord astrocytoma mimicking multifocal myelitis

Abstract Introduction Differential diagnosis of acute/subacute intrinsic spinal cord lesions can be challenging. In addition, intramedullary neoplasms typically show gadolinium enhancement, mass effect, and cord expansion. Case report We report a patient with spinal cord and brain stem lesions resembling multifocal myelitis. Magnetic resonance imaging showed no spinal cord enlargement or gadolinium enhancing. Treatment of myelitis was undertaken without stopping the progression of the disease. Biopsy was made and led to a histological diagnosis of astrocytoma. Discussion Astrocytoma must remain as a possible diagnosis of spinal cord lesions, even without typical characteristics of neoplasms. Furthermore, biopsy should always be considered when diagnosis is uncertain.

Suicidal behaviors are very rare in antiparkinsonian drug trials.

Despite the high rates of depression reported in Parkinsons disease (PD) studies [1], PD patients have relatively low frequencies of suicidal behaviors (SB). PDs unique depression profile, in association with executive deficits, may account for this paradox [1,2]. However, an intriguing increase of SB in PD patients has been described in clinical trials involving sub-thalamic nucleus deep brain stimulation (STN DBS) [3]. Voon reported a significant increase in rates of attempted suicide (0.90%) and successful suicide (0.45%) in 5311 patients undergoing STN DBS for PD [3]. Interestingly, SB frequently occurred in spite of significant motor improvement. Recently, the EARLYSTIM trial [4], designed to compare STN DBS with optimal medical therapy in PD patients with early motor complications, reported an alarmingly high frequency of SB (3.2%) with cases of suicide (3), attempted suicide (4) and suicidal thoughts (1). Importantly, SB frequencies were not significantly different between the two groups. The authors postulated that this increased suicidal risk profile was a trait inherent in patients who qualify for DBS and opt for trial participation testing an invasive treatment, rather than a direct adverse consequence of DBS itself [5]. To investigate an intrinsic suicidal effect of trial participation itself (outside the context of surgical trials), we studied the occurrence of suicidal behaviours in antiparkinsonian clinical trials. We aimed to quantify the frequency of SB reported as adverse events in trials evaluating antiparkinsonian drugs for PD. If clinical trials in general select PD patients more prone to suicidal behaviours, antiparkinsonian trials would report a high frequency of these behaviours. This would contrast with the low frequencies observed in other settings [2]. Additionally, we were interested to know whether any specific antiparkinsonian drug is associated with suicidal behaviours. We performed a systematic review of randomized, paralleldesign, double-blind, placebo-controlled trials evaluating antiparkinsonian drugs (commercial or not) for idiopathic PD, with amajor