G. R. K. Sarma

A case of parkinsonism worsened by losartan: a probable new adverse effect.

We describe a probable new adverse effect of the anti-hypertensive drug losartan in a patient with Parkinson’s disease. The patient is a 65-year-old man with hypertension and Parkinson’s disease that started at 60 years of age. He noticed rest tremors of his left hand 5 years ago, slowness of walking and stiffness of his left sided limbs 3 years ago. Similar symptoms were noticed in the right-sided limbs 2 years back. He noticed tendency to fall backwards for the last 2 years especially while turning around. He was started on a combination of levodopa and carbidopa by his general physician 3 years back and found significant improvement in his walking speed, tremors, and stiffness of his limbs. Tendency to fall did not improve significantly. For the last 1 year, he noticed that the effect of L-dopa has been lasting for shorter duration than before, but he did not report any involuntary movements with L-dopa intake or any unpredictable fluctuations in his motor functions. His clinical features fulfilled the National Institute of Neurological Disorders and Stroke criteria for the diagnosis of Probable Parkinson’s disease. He had been stable on L-dopa/carbidopa (100/25 mg) twice a day and ramipril 5 mg/day. Three months ago, his family physician changed ramipril to losartan 25 mg/day and later increased it to 50-mg/day for better control of hypertension. The patient gradually worsened since then with several falls, freezing episodes, severe bradykinesia requiring constant support of his spouse for activities of daily living. His UPDRS motor score was 50 at the time of admission. We stopped losartan and continued L-dopa in the same doses. After 48 hours, patient made remarkable improvement in bradykinesia, rigidity, and tremors. He was walking independently and had only occasional brief freezing episodes. His UPDRS motor score improved to 39. To establish the causal relationship of losartan to the parkinsonism symptoms, we re-challenged the patient with losartan 25 mg/day. After 48 hours, patient deteriorated again with severe bradykinesia and frequent freezing episodes. His UPDRS motor score worsened to 50 again. We discontinued losartan again. Twenty four hours later, patient was ambulating independently, with mild bradykinesia and occasional brief freezing. His UPDRS motor score improved to 41. Patient’s blood pressure was later controlled with ramipril 10-mg/day. Losartan is an angiotensin receptor blocker. There is experimental evidence to suggest that Angiotensin facilitates nigrostriatal dopaminergic release by acting on Angiotensin receptor type 1.1–3 Losartan blocks these receptors and inhibits dopaminergic release. Angiotensin converting enzyme inhibitors like ramipril, on the contrary, may facilitate dopaminergic release.4 The half-life of losartan is very short, about 2 hours. This may explain the rapid improvement that was seen in this patient after discontinuation of losartan. To our knowledge, this is the first report of parkinsonism worsened by losartan. Applying Naranjo’s algorithm, the present adverse event can be considered as “probable” effect of losartan. Further evidence is needed for clearly establishing the relationship between angiotensin receptor blockers and parkinsonism. It cannot be over emphasized that such information is most relevant in the treatment of Parkinson’s disease associated with hypertension.

Acute painful peripheral neuropathy due to metronidazole.

372 CMYK limbs versus the lower extremities (cruciate palsy, brachial diplegia) is seen in the traumatic central cord syndrome or cervical spondylotic myelopathy of elderly patients. Brachial diplegia due to pyramidal tract involvement was first described by Mohr, while the term man-in-the-barrel syndrome (MIBS) was coined by Sage and Van Clitert to describe the clinical aspect of the patient with disproportionate weakness of both arms, while maintaining mobility of face and lower limbs (as though the trunk of the patient is stuck on a barrel). The term cruciate palsy is best used for lesion of corticospinal tracts in the medulla, while exclusive use of the term MIBS for bilateral frontal lobar lesions as in the original description would provide more clarity to the terminology. MIBS is seen commonly after cardiac tamponade, aortic surgery, systemic hypoperfusion and hypovolaemic shock, head injury, anoxic damage to the cortex in the area of somatotopic representation of the arms. There is only one report of tumors being responsible for MIBS – that due to cerebral metastases from undifferentiated carcinoma lung. Multicentric glioma presenting as MIBS has not been reported earlier.

Dot sign in dengue encephalitis

Neuro radiological findings in Dengue encephalitis are non specific .Here we report a case of Dengue encephalitis with transient splenial hyperintensity appearing as dot sign on magnetic resonance imaging of brain.

Boomerang sign in rickettsial encephalitis.

A 17‐year‐old male had high‐grade fever for five days. On day 5 of fever, he developed maculopapular pruritic rashes all over the body including palms and soles. Later he developed frontal headache, nausea and vomiting followed by altered sensorium. There was mild enlargement of liver and spleen. Neurological examination revealed a drowsy patient with neck stiffness and left oculomotor palsy. Cerebrospinal fluid showed ten lymphocytes and elevated proteins with normal sugars. Blood tests for malaria, dengue and leptospirosis were negative. Weil‐Felix reaction showed rising titers for Ox‐K antigen. MRI brain diffusion weighted image (DWI) showed lesions with restricted diffusion in the splenium and genu of the corpus callosum [Figure 1]. On apparent diffusion coefficient (ADC) mapping, these lesions had low apparent diffusion coefficient [Figure 2]. Magnetic resonance imaging‐fluid‐attenuated inversion recovery/ T2w (MRI FLAIR/T2w) imaging showed hyperintense lesions in the splenium of corpus callosum [Figure 3]. However, the hyperintensity was less prominent in these sequences when compared to DWI and ADC images. The lesion was hypointense on T1w image [Figure 4] and did not show any enhancement on contrast administration [Figure 5]. The splenial lesion mimicked

SUNCT syndrome treated with gamma knife targeting the trigeminal nerve and sphenopalatine ganglion

SUNCT syndrome, an abbreviation for short lasting-unilateral neuralgiform headache attacks with conjunctival injection and tearing is one of the most debilitating unilateral headache syndromes often refractory to medical therapy [1]. We report a case of a 50-year-old man diagnosed with refractory SUNCT syndrome having a near complete response to gamma knife surgery targeting the trigeminal nerve and sphenopalatine ganglion.

Temporal arteritis: A case series from south India and an update of the Indian scenario

Objective: To study the clinical, pathological and prognostic profile of patients with temporal arteritis in India. Materials and Methods: The study was conducted in a tertiary care center from south India from 2005 to 2010 in the departments of neurology and medicine. The details of all patients that satisfied the ACR 1990 criteria for diagnosis of temporal arteritis were reviewed. The clinical presentation, laboratory parameters and biopsy findings of the patients were analyzed and compared with other studies from India done over the last decade. Results: A total of 15 patients were diagnosed with temporal arteritis. The male:female ratio was 1.5:1. The mean age of onset was 67.58 years. Mean time for detection after onset of symptoms was 2.56 months. Typical manifestations included headache (100%), temporal artery tenderness (100%), jaw claudication (20%), polymyalgia rheumatica (53%) and visual manifestations (20%). The erythrocyte sedimentation rate was elevated in all patients. Biopsy was done in 13 patients, with 11 of them being positive. All patients responded to steroids well, with most patients being symptom-free within the first 48 h of treatment. Conclusions: Temporal arteritis seems to be underdiagnosed in India, with all patients previously misdiagnosed, and with a mean time from symptom onset to diagnosis of 2.5 months. The clinical presentation of temporal arteritis in India appears to be similar to that of the West, with no gender preference and a slightly younger age group.

Trigeminal autonomic cephalalgia as a presenting feature of Neuromyelitis Optica: "A rare combination of two uncommon disorders".

Neuromyelitis Optica (NMO) can have atypical presentations like hiccups, vomiting, etc. which is classically described as the area postrema syndrome. Here we report a case of a 39 year old male patient who presented with features of Trigeminal Autonomic Cephalalgia (TAC). MRI spine showed long segment myelitis. Diagnosis of NMO was confirmed by a positive Anti aquaporin 4 antibody assay. TACs are a rare group of headache disorders characterized by severe unilateral headache in the V1 distribution of the trigeminal nerve and autonomic symptoms. This presentation in NMO is hitherto unreported in literature.

Seasonal and monthly trends in the occurrence of Guillain-Barre syndrome over a 5-year period: A tertiary care hospital-based study from South India.

Annals of Indian Academy of Neurology, April-June 2014, Vol 17, Issue 2 included or not remains unclear from the available description. No objective test (e.g. urinalysis) was employed to rule out concurrent substance abuse, in particular, benzodiazepine use, which has the potential to induce withdrawal seizures similar to alcohol. It has been mentioned that all subjects gave informed wri en consent to participate in the study; however, some patients had delirium as reported in the paper. From an ethical perspective, a mention must be made of the consent from a legal guardian. Table 1 shows mean time interval between alcohol intake to seizure (19.35 ± 35.94 h) where the standard deviation is quite high compared to the mean. Instead, median and range would have conveyed be er information on variance or dispersion from mean.

Hurdles in stroke thrombolysis: Experience from 100 consecutive ischemic stroke patients

Background: Acute management of ischemic stroke involves thrombolysis within 4.5 h. For a successful outcome, early recognition of stroke, transportation to the hospital emergency department immediately after stroke, timely imaging, proper diagnosis, and thrombolysis within 4.5 h is of paramount importance. Aim: To analyze the obstacles for thrombolysis in acute stroke patients. Materials and Methods: The study was conducted in a tertiary care center in South India. A total of hundred consecutive patients of acute ischemic stroke who were not thrombolysed, but otherwise fulfilled the criteria for thrombolysis were evaluated prospectively for various factors that prevented thrombolysis. The constraints to thrombolysis were categorized into: i) Failure of patient to recognize stroke symptoms, ii) patient′s awareness of thrombolysis as a treatment modality for stroke, iii) failure of patient′s relative to recognize stroke, iv) failure of primary care physician to recognize stroke, v) transport delays, vi) lack of neuroimaging and thrombolysis facility, and vii) nonaffordability. Results: The biggest hurdle for early hospital presentation is failure of patients to recognize stroke (73%), followed by lack of neuroimaging facility (58%), nonaffordability (56%), failure of patient′s relative to recognize stroke (38%), failure of the primary care physician to recognize stroke (21%), and transport problems (13%). Awareness of thrombolysis as a treatment modality for stroke was seen only in 2%. Conclusion: Considering the urgency of therapeutic measures in acute stroke, there is necessity and room for improvement to overcome various hurdles that prevent thrombolysis.

Author's Reply: "Dot sign" in dengue encephalitis

1. Mathew T, Badachi S, Raja G, Nadig R. “Dot sign” in dengue encephalitis. Ann Indian Acad Neurol 2015;18:77-9. 2. Ventureyra EC, Abdel Aziz H. The “dot sign”. Pediatr Neurosurg 2001;35:111. 3. Thomas B, Kesavadas C. Neurological picture. Focal splenial hyperintensity in epilepsy. J Neurol Neurosurg Psychiatry 2006;77:202. 4. Sen K, Guha G, Khandelwal K, Lalhmachhuana J. The enigma of transient splenial hyperintensity: In cryptococcal meningitis. J Neurosci Rural Pract 2013;4:352-5. 5. Verma R, Sahu R, Holla V. Neurological manifestations of dengue infection: A review. J Neurol Sci 2014;346:26-34. Sir, The recent report on “Dot sign and dengue encephalitis” is very interesting.[1]The finding of dot sign in diagnosis of dengue encephalitis should be commented. In this case, “transient splenial hyperintensityappearing asdot sign in magnetic resonance imaging (MRI)” is mentioned.[1] Indeed, “dot sign” is classically mentioned in some diseases, but not infectious disease as dengue.[2] Transient splenial hyperintensitycan be seen in many neurological problems such as cryptococcal meningitis[3] and epilepsy.[4] The concomitant disorder in the present case is questionable. Indeed, dengue encephalitis is an uncommon neurological presentation of dengue and the clinical features can hardly be differentiated from other encephalitis.[5] The MRI seems to be not helpful for definitive and differential diagnosis.[5]