Background: Ramsay Hunt Syndrome with cerebellar encephalitis is rare in adult. Case Report: We describe a 55-year-old diabetic female who presented with truncal ataxia, right peripheral facial palsy and right ear pain associated with erythematous vesicular lesions in her external auditory canal. Later, she developed dysmetria, fluctuating diplopia and dysarthria. No facial lesions were identified and lesions were limited to the external auditory canal. Cerebral spinal fluid tested positive for varicella zoster virus polymerase chain reaction. She was diagnosed with Ramsay Hunt Syndrome with spread to the central nervous system and treated with acyclovir intravenous therapy (10 mg/kg every 8 hours). Her facial palsy completely resolved within 48 hours of acyclovir treatment, however, vesicular lesions, imbalance and cerebellar symptoms remained; a tapering course of high dose prednisone was then added.

Discussion: Prognosis for facial palsy is poor in Ramsay Hunt Syndrome: Only 10% of patients will have complete resolution of their facial palsy. Improvement of facial palsy may be a good marker for response to treatment. Conclusion: Varicella zoster virus reactivation affecting the central nervous system in adults is rare. Knowledge of Ramsay Hunt syndrome with brainstem and/or cerebellar involvement is important for diagnosis and for consideration of antiviral and prednisone treatment.

Objective: To compare and contrast the observed versus predicted number of white blood cells (WBCs) in a traumatic cerebrospinal fluid (CSF) sample in children and adults. Background: Clinicians rely on a correction formula (Predicted_CSF_WBC=CSF_RBC×Blood_WBC/Blood_RBC) to determine if a true CSF leukocytosis exists. This formula may overestimate true CSF leukocytosis and lead to delayed treatment of meningitis. Methods: A retrospective review of CSF data of 105 patients who met the following criteria: 1) CSF from lumbar puncture (LP) contained≥1000 RBC/mm^3 and 2) CBC performed≤24 hours of LP; 3) negative CSF cultures. Regression analysis was performed to determine the relationship between actual and predicted CSF WBC values. Results: Regression modeling indicated a discrepancy in the predicted versus actual WBC values. Mean adult age was 48.9 years; CSF profile (mean WBC 146.3×10^6/L; RBC 17374×10^6/L; glucose 4.1 mmol/L; protein 1.4 g/L); mean peripheral WBC was 8.2×10^9/L; RBC 3.9×10^9/L. Mean pediatric age was 1.4 years; CSF profile (mean WBC 171.8x10^6/L; RBC 41763x10^6/L; glucose 2.7 mmol/L; protein 1.7 g/L); mean peripheral WBC was 12×10^9/L; RBC 7.2×10^9/L. Observed LP CSF WBC value was 47% of predicted (r^2=0.54 pediatric cohort; r^2=0.91 adults). Conclusion: True CSF leukocytosis could be missed in a traumatic CSF sample based on a currently applied correction formula. We propose the following modifcation: Observed_CSF_WBC=0.5x[CSF_RBC×Blood_WBC/Blood_RBC].

Background: The Alzheimer’s Disease Neuroimaging Initiative (ADNI) provides an opportunity to investigate the relationship between β-Amyloid neuropathology and patients’ long-term cognitive function change. We examined baseline 18F-florbetapir PET amyloid imaging status and 36-months’ change from baseline in cognitive performance in subjects with mild cognitive impairment (MCI). Method: The study included all ADNI subjects who underwent PET-imaging with 18F-florbetapir and had a clinical diagnosis of MCI at the visit closest to florbetapir imaging. β-Amyloid deposition was measured by florbetapir standard uptake value ratio (SUVR), and dichotomized as Aβ+(SUVR>1.1) or Aβ–(SUVR≤1.1). Cognitive scores, including ADAS11, MMSE and CDR sum of boxes (CDR-SB), were evaluated for up to 36 months. Results: Of 478 MCI-subjects who had at least one florbetapir scan, 153 had a cognitive evaluation at 36-month follow-up. Of those, 79 were Aβ– and 74 Aβ+. At 36-months, the Aβ+ vs. Aβ– group scores changed from baseline (LS means 4.03 vs. 0.26 for ADAS11; -2.61 vs.-0.40 for MMSE; 1.53 vs. -0.11 for CDR-SB [p< 0.0001 all comparisons]). Generalised estimating equation analysis on clinically significant cognitive change showed a marginal Odds Ratio=2.18 (95% CI: 1.47–3.21) for Aβ+ vs. Aβ– groups. Conclusion: MCI subjects with higher β-Amyloid deposition had greater deterioration in cognitive function over 36 months while subjects with no β-Amyloid accumulation tended to be stable.

Background: Opsoclonus can result from paraneoplastic, parainfectious, autoimmune, ischemic or toxic etiologies. Neuroinvasive complications develop in less than one percent of individuals infected with West Nile Virus. Methods: Case report. Results: A 63-year-old female presented with subacute disorientation, dizziness, oscillopsia, and unsteady gait, associated with fever. Examination demonstrated opsoclonus, bilateral upper extremity postural and action tremor and truncal ataxia. MRI of the brain was normal. CT of the body showed no evidence of neoplasia. Vasculitic and paraneoplastic panels were negative. An extensive infectious work-up was only positive for West Nile IgM antibodies. She was treated with clonazepam and received a five-day-course of IVIG. Her symptoms improved after treatment and she continued to demonstrate gradual recovery during the months following her discharge. Conclusions: There are only a few published case reports of WNV-associated opsoclonus, and our patient appears to be the oldest reported with this constellation of neurological symptoms. Even though treatment for WNV is mostly supportive, this case demonstrates the importance of a thorough work-up in patients of similar presentations to determine the etiology and to guide early immunomodulation in selected cases. Video available.

The objectives of the study were to analyze the association between Parkinson’s disease and restless legs syndrome, and explore the relationship between mood disorder comorbidity (anxiety and depression), pain, and restless legs syndrome. This study included 123 Parkinson’s disease patients and 123 healthy controls matched for age and gender, and evaluated for anxiety severity, depression severity, pain severity, pain interference, pain disability, and restless legs syndrome prevalence. This was performed using semi-structured interviews and a neurological examination. Restless Legs Syndrome diagnostic criteria and the following inventories were used; Hospital Anxiety and Depression Scale, Brief Pain Inventory, and Pain Disability Index. Parkinson’s disease patients had significantly greater anxiety severity, depression severity, pain severity, pain interference, pain disability, and restless legs syndrome prevalence in comparison to controls. In addition, Parkinson’s disease patients’ comorbid for anxiety and depression had significantly greater pain severity, pain interference, and pain disability, but not RLS prevalence, in comparison to Parkinson’s disease only, Parkinson’s disease anxiety, and Parkinson’s disease depression patients. Pain interference, pain severity, and pain disability is greater among Parkinson’s disease patients with anxiety and depression, in comparison to Parkinson’s disease patients without anxiety and depression. On the contrary, the prevalence of restless legs syndrome was not found to be relevant.

Objective of this study was assess the prevalence of Essential of Essential Tremor in Parkinson’s disease population Essential tremor (ET) is the most common movement disorders and is much more common than Parkinson’s disease, in general population. Essential Tremor and Parkinson’s disease (PD) tremor differ in type, frequency and distribution. Despite being two separate disorders, there have been cases reported of coexistence of ET-PD. Some studies have reported an increase in the incidence of ET in relatives of patients with PD, yet the risk of developing PD in ET patients has not been thoroughly investigated. Our study set out to determine the prevalence of precedent ET in PD patients. We conducted a retrospective chart review analysis of 332 idiopathic PD patients to determine how many of them had ET prior to the diagnosis of PD and the percentage of them who were also diagnosed with ET. Our results indicated that the prevalence of precedent ET among a population of idiopathic PD patients was not any higher than the prevalence of ET in a comparable general population. Our results support the notion that ET and PD are mutually independent disorders. Further studies are needed to understand the exact relationship between these two disorders

Background: We present clinical and MRI features of progressive ataxia and palatal tremor (PAPT). Case Report: A 67 year-old gentleman visiting from Vietnam presented with intermittent stroke-like episodes consisting of facial weakness, dysarthria, and osillopsia. He reported gradually worsening ataxia and dysequilibrium over 4 years. Examination revealed small amplitude nystagmus towards the right, impaired VOR to the left, palatal tremor, left-sided dysmetria, and an unsteady gait. MRI of the brain demonstrated increased T2/FLAIR signal within the inferior olive. Contrast enhanced and diffusion sequences were normal. MRA was normal. Electrocardiography, telemetry, and echocardiogram were normal. CSF was normal. Glial fibrillary acidic protein (GFAP) and vitamin E levels were normal. Genetic testing for hereditary forms of ataxia including spinocerebellar ataxia was not completed. Conclusion: Palatal tremor is commonly classified into symptomatic or essential subgroups. Symptomatic palatal tremor is frequently caused by a lesion in the triangle of Guillain and Mollaret leading to hypertrophic olivary degeneration. A subgroup of symptomatic palatal tremor form a syndrome of PAPT. Published details of cases of PAPT are sparse and the disorder appears to be mainly sporadic. Common features include progression of ataxia, olivary degeneration, gaze-evoked nystagmus, and internuclear ophthalmoplegia. There is no known effective treatment for progressive ataxia, which is the most disabling symptom of PAPT.

Objectives: The objectives of this study are to understand the impact of natalizumab on cognition beyond two years of therapy and to investigate whether baseline characteristics are predictive of clinical response. Methods: This is a single-center, 24-month, observational study. Sixty-three patients treated with natalizumab were assessed prior to monthly infusions using a Cogstate battery and the SDMT. A linear mixed model was conducted with duration of natalizumab therapy as a between-subjects factor (<=2 or >2 years), assessment as a within-subjects factor, and MSSS as a covariate. Results: There were no statistically significant differences between the key demographic variables aside for the MSSS (p=.0074). No patient showed evidence of sustained cognitive deterioration over the 24 month period. Irrespective of time on natalizumab, significant improvements were observed at the group level in executive function, verbal memory and working memory, whereas processing speed and attention remained unchanged. Impaired cognition or any other baseline parameter did not influence the trajectory of cognitive change over 24 months. Conclusion: Our results suggest that natalizumab preserves cognitive function, including the ability to learn, for 4 years and beyond of continuous therapy. This occurs irrespective of baseline characteristics.

Background: Risk of progressive multifocal leukoencephalopathy (PML), a serious adverse event of natalizumab therapy, is higher with positive anti-JC virus antibody status, greater cumulative exposure to natalizumab and prior immunosuppressant use. Plavina et al. (2014) showed that plasma or serum anti-JC virus antibody index value may allow further PML risk stratification. Among anti-JC virus antibody positive multiple sclerosis patients with no prior immunosuppressant treatment receiving natalizumab, anti-JC virus antibody index >6 months prior to PML diagnosis was significantly higher among those who developed PML with 96% consistently having an anti-JC virus antibody index >0.9. Methods: We describe a case of natalizumab-associated PML with low positive anti-JC virus index value prior to diagnosis. Results: A 53 year old man with 20 year history of relapsing remitting multiple sclerosis was diagnosed with PML following 46 infusions of natalizumab. Glatiramer acetate was his only prior immunomodulatory therapy. Routine MRI surveillance resulted in diagnosis of PML following detection of a confluent right anterior frontal T2 hyperintense lesion extending across the corpus callosum. Six months prior, routine MRI surveillance demonstrated a small right frontal T2 hyperintensity with no diffusion restriction while serum anti-JC virus antibody index was 0.69. Conclusions: Natalizumab-associated PML may develop despite low positive anti-JC virus index value.

Background: Multiple sclerosis (MS) exhibits a spectrum of clinical findings, especially in relapsing-remitting MS (RR-MS). To assess the effects of geographic location and ethnicity on RR-MS phenotype, we investigated RR-MS patients in Canada and Saudi Arabia. Methods: A retrospective cross-sectional analysis of patients receiving active care in MS Clinics was performed in Medina, Saudi Arabia and Edmonton, Alberta. Demographic and clinical data was collected for each patient. Results: 98 patients with treated RR-MS were recruited (n=51, Medina; n=47, Edmonton); 40 patients were Caucasian (Edmonton) while 46 patients were Bedouin (Medina). Although the disease duration was longer in the Edmonton (5.7+2.3 yr) compared to the Medina group (4.4+1.4 yr) (p<0.05), the mean age of RR-MS onset, relapse rate and EDSS change were similar. The female:male ratio was comparable in Edmonton (35:12) and Medina (32:19), as was the risk of optic neuritis. The likelihood of an infratentorial lesion-associated presentation differed (Edmonton, n=23; Medina; n=13) among groups (p<0.05). Spinal cord lesions on MRI were more frequent in Edmonton (n=18) compared to Medina (n=1) patients (p<0.05). Conclusions: Despite differences in location, ethnicity, and a predominance of infratentorial lesion burden the Edmonton group, the RR-MS phenotype displayed similar disease severity and trajectory in these cohorts.

Background: The beneficial effects of the injected disease-modifying drugs (DMDs) in relapsing-remitting Multiple Sclerosis have been previously reported. However the results related to disability outcomes and the reduction of disease progression in the pivotal trials and few longer studies are variable and inconclusive. Objectives: To determine the utilization and the disability outcomes of the DMDs on relapsing-remitting Multiple Sclerosis over fifteen years. Methods: A prospective open-label cohort of 262 clinical definite patients, 78 men and 184 women, with two attacks in the past two years and a disability level DSS≤5.5 were enrolled consecutively from December 1997 to November 1999. A descriptive analysis of the cohort and individual drugs outcomes were performed. The results were compared to natural history studies of Multiple Sclerosis as controls. Results: At 15 years, one-seventh, 38/262 (14.5%) remain on the initial prescription, Betaseron, 15/131 (11.5%), Copaxone, 16/102 (15.5%) and Rebif 7/28 (25%), Avonex 0/1. 223(63.6%) had discontinued at a mean duration of 5.5(SD=4.7) years. 95/262 (36.4%) remain on a drug after switches. The DSS levels of the individual DMDs were analyzed. Conclusion: One-seventh of participants remained on their first prescription. Because of low adherence, the impact of DMDs on disease progression in the longer term cannot be verified.

Objectives: To investigate if MS subjects treated with PRF 10mg BID will show a greater benefit from active enabled motor training compared with placebo. Methods: Single center, phase 4, pilot, placebo-controlled, double-blind 18 weeks study. Fifteen patients were randomized to receive PRF 10 mg BID and fifteen to received placebo BID. All patients participated in active enabled motor training of 3 sessions of 1 hour/week for 6 weeks. Patients were evaluated at -4, 0, 6 and 14 weeks using the timed 8 meters walk (8 MW), the 6 minute walk (6 MW) and the timed sit to stand (STS). Results: The PRF treated group achieved a higher mean percent improvement from baseline in all tasks at both 6 and 14 week time points. The difference reached statistical significance (mean difference of 14.29, p=0.046) for the 8MW at the 14 week time point. A higher incidence of responders (>20% improvement from baseline) was seen in the PRF treated group at 6 weeks on the 8MW (odds ratio [OR] of 2.31) and the 6MW (OR of 1.63), and at 14 weeks on the 8MW and the STS (OR of 2.0). Conclusions: PRF in MS patients appears to enhance the benefit of active enabled motor training and to better sustain it over the following 8 weeks.

Background: Donation after circulatory death (DCD) can reduce organ transplant waiting times. When defining death using circulatory criteria, brain function is usually not assessed. Residual brain function and the state of consciousness at the time of circulatory arrest is unknown. We have an ethical responsibility to ensure the donor is free of pain and psychological distress. Methods: We performed a scoping review of the literature to determine the time intervals associated with the loss brain function after circulatory arrest. Results: A total of 1133 articles were reviewed and 38 were included in the review. In humans, 8 studies showed loss of EEG activity under 30 seconds. Four studies revealed loss of EEG between 39.6 and 66 seconds. Clinically, loss of consciousness was shown to occur between 4 and 21 seconds. In animals, 13 studies also revealed loss of EEG under 30 seconds. In four other animal studies, EEG was lost between 37 and 120 seconds. Conclusion: The time required to lose brain function varied according to clinical context and method by which this function is measured. Existing literature is scarce and limited to observational studies and case reports.

Objective: Case report of NMDA receptor encephalitis in a young man with early refractory status epilepticus and atypical radiological findings. Background: Anti-NMDA receptor encephalitis is an autoimmune disorder due to antibodies to the NR1-NR2B heterodimer of NMDA receptor. On imaging, it typically presents with T2 hyperintensities in mesio-temporal lobes, cerebral cortex and basal ganglia. We present a case with a dramatic clinical evolution and novel imaging findings. Design/Methods: Case report and review of imaging. Results: 29-year-old male presented with mood disturbance followed by partial-complex seizures, facial dyskinesia and choreo-athetotic movements. Initial MRI showed subtle T2-hyperintensities in mesio-temporal lobes. Diagnosis of NMDA-receptor encephalitis was confirmed after CSF antibody detection. Prior to diagnostic confirmation, he developed refractory status epilepticus, and concomitant signs of herniation. A repeated MRI showed increased T2-hyperintensities of thalami and mesencephalon, with cerebellar involvement and transtentorial/foraminal herniation. Restricted diffusion was documented in the cerebellar cortex/thalami/putamina and caudate. IV corticosteroids and hypertonic fluid reversed herniation, and halted the seizures. Conclusions: To our knoweldge, we report the first case report of uncal and tonsillar herniation in NMDA-r encephalitis secondary to atypical, predominant cerebellar involvement. This case highlights life-threatening manifestation that physicians might encounter, and a possible role for high dose IV corticosteroids as an adjunct treatment for brain edema and seizures.

Background: IL-27 acts as a ‘master regulator’ in modulating inflammation and was responsible for a number of autoimmune diseases. However, the role of IL-27 was not addressed in Guillain-Barré syndrome (GBS). Methods: Sixty-five subjects including 19 with GBS, 7 with encephalitis or meningitis, 23 with multiple sclerosis or neuromyelitis optica as well as 11 with other non-inflammatory neurological disorders were enrolled. ELISA was used to detect the concentrations of IL-27 in paired samples of cerebrospinal fluid and plasma. Results: The mean concentration of IL-27 in GBS patients was significantly lower than in other neurological disorders both in CSF and in plasma (all p<0.05). GBS patients with cranial involvement, decreased reflexes, hypaesthesia, autonomic nerve dysfunction, MRC score <30 are inclined to have a lower CSF IL-27 level than patients without these symptoms (182 pg/ml, 181 pg/ml, 185 pg/ml, 185 pg/ml, 194 pg/ml vs 211 pg/ml, 205 pg/ml, 202 pg/ml, 198 pg/ml, 199 pg/ml, respectively). Similar results were noted in plasma except for cranial involvement. Conclusions: Production of IL-27 was disparate between GBS and other neurological diseases and a significantly lower level of IL-27 was observed in GBS patients, indicative of an anti-inflammatory role of IL-27 in GBS.

Background: Dysphagia from ALS may be treated by enteral nutrition; however criteria for timing of feeding tube placement has not been well studied. The aim of this project was to better understand the practice of enteral nutrition management within Canadian ALS clinics. Methods: ALS clinics were asked if they had written guidelines for timing of PEG insertion and if not, what criteria they use to make this decision. Results: Responses from 10 of 17 clinics were received. One clinic had written guidelines. Most used decline in respiratory function, dysphagia, weight loss or some combination of all three. Six clinics reported dropping FVC, ranging from 70% to 50% as prompting tube insertion. Five clinics reported weight loss as part of their criteria. Dysphagia was reported as the most important factor by 7 clinics. Psychological readiness for tube placement was a key factor in 3 clinics. Some clinics comment they place tubes in advance of dysphagia. Conclusion: Criteria for tube insertion varies between clinics. Practices generally reflect published recommendations, but vary on the emphasis of specific criteria. The lack of strong scientific evidence to guide decisions may contribute to management variability. Further study is needed to guide practice.

Background: In Charcot-Marie Tooth (CMT), vital components of either the myelin sheath or axon are abnormal, slowing nerve conduction and causing functional disability. Recently, there has been speculation the CMT may have an autoimmune component resulting from abnormal protein expression. Methods: Custom autoimmune neuropathy-focused microarray panels were printed in-house using antigens from Sigma, Abnova, Fitzgerald and Matreya according to Cambridge Life Science instructions. Antigens including Myelin Protein Zero, Peripheral Myelin Protein 22, and 20 other well-known gangliosides were tested for IgM and IgG antibodies. Students T-Test and Bonferroni correction factor were used to determine statistical significance between groups and in post-hoc subgroup analysis. Results: Plasma was tested from 17 patients with CMT and 25 young healthy individuals. CMT population consisted of 9 CMT-1a, 1 CMT-1b, 4 CMT-2a, 2 CMT-2f and 2 undetermined CMT type 2 patients. No ganglioside reached statistical significance under a Bonferroni Correction factor (p>0.01) nor were any gangliosides notably raised compared to normal. Sub-group analysis did not reveal theorized peak auto-antibodies levels depending upon their CMT sub-type compared to normal. Conclusions: Although previously shown to have increased auto-antibodies to myelin or axonal proteins, CMT individuals did not demonstrate increased autoantibody levels for the proteins tested at our centre.

Background: The response of Chronic Inflammatory Demyelinating Polyneuropathy ( CIDP ) to Intravenous Immunoglobulins (IVIG) treatment is well established. However, determination whether patients who do not respond to 2 IVIG treatments or those whose condition stabilizes (ICE Trial) would benefit from additional treatments remains unclear. We aim to identify time period required to reach maximal strength gains from IVIG treatment (plateau). Furthermore, we will assess nerve conduction studies (NCS) changes over time with IVIG treatment. This will help in establishing a time course for treatment of CIDP with IVIG to maximize recovery. Methods: We performed a retrospective chart review of 27 patients with CIDP, with diagnosis confirmed by European Federation of Neurological Societies/Peripheral Nerve Society Guidelines (EFNS/PNS). Each patient’s strength response including: grip strength, knee extension, elbow flexion and dorsiflexion (using JAMAR Dynamometer) and NCS changes over time during IVIG treatment were analyzed. The primary outcome is duration of IVIG treatment, in months, required to reach a plateau in strength. Secondary outcome is NCS change including: Terminal Latencies, Conduction Velocities, Compound Sensory and Motor action potentials in nerves of upper and lower extremities over treatment time (emerging trends). Results: Pending (available by April 2015) Conclusion: Pending (available by April 2015)

Aim/Background: We report a case of Acute Combined Central and Peripheral Demyelination (ACCPD). This rare disease presents with features of both peripheral and central demyelination. Methods: Case Report Results: A 24 year-old Iraqi female presented with acute onset of ascending paralysis, numbness and areflexia over the course of a few days. Systemic examination was negative. She responded to IVIG. She suffered two severe relapses over the next three months, which resolved rapidly with PLEX/corticosteroid. CSF was normal after first and second relapses. Brain and cord MRI revealed multiple T2/FLAIR hyperintensities consistent with multiple sclerosis. There were no longitudinally extensive cord lesions. Aquaporin 4 antibody assay is pending. ANA was strongly positive; anti-DSDNA and SS antibodies were negative; complement4 was low and serum cyroglobulins were positive. Hepatitis C was negative. Ganglioside antibody assay was negative. Anti-neurofascin is pending. Neurophysiology confirmed features of an acquired demyelinating neuropathy with profound secondary axonal denervation. Conclusions: The underlying etiology of ACCPD is presumed autoimmune likely secondary to auto-antibody targeting of central and peripheral myelin epitopes. Low complement component 4 and cryoglobulinemia in this patient supports an autoimmune pathogenesis. Neurofascin has been previously reported as one such auto-antibody in ACCPD.

Background: Our study examined whether there are differences in MS mortality rates across regions of Canada, which might suggest differences in environment or health care practice that influence outcome. Methods: Statistics Canada data on deaths due to MS and populations at risk, 1975-2009, were derived from the Research Data Centre, University of Alberta. Mortality rates and 95% confidence intervals (CIs) were calculated per 100,000 population for the Atlantic Provinces, Quebec, Ontario and Western Provinces (including Northwest Territories, Yukon, Nunavut), age-standardized to the 2006 population. Results: The average annual MS mortality rates for 1975-2009 per 100,000 population (CIs) were: Atlantic Provinces 1.09 (0.43,1.74); Quebec 1.30 (0.89,1.71); Ontario 1.08 (0.77,1.38); Western Provinces 1.39 (0.99,1.78). Female mortality rates were consistently higher than male rates but there were no differences in the female:male mortality rate ratios across regions. Trend analysis showed that rates were stable over the 35 year time span in 3 regions with non-significant average annual per cent increases/decreases of: Atlantic Provinces –0.43%; Quebec +0.12%; and Western Provinces +0.27%. Only Ontario showed a slight but significant increase of +0.81% (p<0.05). Conclusions: MS mortality rates are similar across the Canadian regions, suggesting that patients are not disadvantaged in terms of mortality by their place of residence.