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AimsThe urinary dysfunction in multiple system atrophy (MSA) is characterized by large post-void residuals (PVR) due to impaired bladder contractility. However, the evaluations of bladder contractility are not well validated in MSA. Because the bladder contractility index can be generally represented as Pdet Qmax (detrusor pressure at maximum urinary flow rate) + kQmax (maximum urinary flow rate), we aim to examine which “k” value is suitable for representing bladder contractility concerning its correlations to PVR and voided percentage (VOID%).MethodsWe retrospectively reviewed 133 patients with MSA (74 males, 59 females, mean disease duration 3.2 years) who underwent an urodynamic study. We calculated bladder contractility using the formula PIPk = Pdet Qmax + kQmax by increasing the “k” value from 0.1 to 10 by increments of 0.1. We calculated the correlations between each PIPk (k = 0.1–10.0) and PVR and VOID%.ResultsThe correlational coefficients between PIPk and VOID% were larger than those between PIPk and PVR. The correlational coefficients between PIPk and VOID% reached a plateau level at a “k” value >5.0 in male patients, suggesting that currently used formulas such as Pdet Qmax + 5Qmax for males might be appropriate for male MSA patients. However, the correlational coefficients between PIPk and VOID% reached a plateau level in female patients when the “k” values were >6.0, which might overestimate bladder contractility in female patients.ConclusionAlthough currently used formulas such as Pdet Qmax + 5Qmax might be appropriate for male MSA patients, formulas for female patients need further evaluation.

This is the third manuscript from the Neuro-urology Promotion Committee of the International Continence Society (ICS) discussing uncommon neuro-urological conditions that are not well described in urological literature. Readers are referred to the previous documents for a more detailed understanding of how neurological disease might affect lower urinary tract function ( https://doi.org/10.1016/j.cont.2022.100022) ( https://doi.org/10.1016/j.cont.2023.101043). Eleven conditions are covered. This includes five genetic conditions — Angelman disease, spinocerebellar ataxias, Fabry’s disease, neurofibromatosis and spinal muscular atrophy. Two infection associated conditions are covered including Human T-lymphotropic Virus Type 1 associated myelopathy/ tropical spastic paraparesis and Creutzfeldt–Jackob disease. Four other conditions covered are cerebral palsy, Lennox–Gastaut syndrome, idiopathic normal pressure hydrocephalus and spinal vascular malformation. Key aspects and specific recommendations related to clinical practice are summarized in tables. Knowledge of unusual neurological conditions that can affect the lower urinary tract is important for ensuring a timely and precise diagnosis. This document from the ICS, along with Parts I and II published earlier, can serve as a reference for clinicians presented with unusual forms of neurogenic lower urinary tract dysfunction.

The medial prefrontal cortex (mPFC) regulates bladder contractions via the periaqueductal grey (PAG). Subthalamic nucleus deep brain stimulation (STN-DBS) modulates urinary afferent information from PAG in Parkinson’s disease (PD). We do not know how STN-DBS modulates the activities of mPFC induced by PAG stimulation. We aim to clarify how STN-DBS modulates the neuronal activity of mPFC induced by PAG stimulation and its effects on bladder contraction Experiments were conducted under urethane anesthesia in normal (n = 9) and 6-hydroxydopamine hemi-lesioned PD rats (n = 7). Left-sided PAG stimulation and STN-DBS were applied with simultaneous bladder contraction monitoring. Local field potential (LFP) recording and collection of extracellular fluid in the mPFC were performed before stimulation, during PAG stimulation, during PAG+STN stimulation, and after stimulation. The bladder inter-contraction intervals significantly decreased with PAG stimulation with a concomitant decrease in mPFC LFP power in PD rats. Adding STN stimulation to PAG stimulation significantly increased the bladder inter-contraction intervals with a concomitant increase in mPFC LFP power in PD rats. Several mPFC catecholamine levels were modulated by PAG or PAG+STN stimulation in PD rats. The present study revealed that STN-DBS modulate the activities of mPFC induced by PAG, thereby leading to normalization of bladder contraction.

Aims:: To summarize recent evidence and practice recommendations from a literature review of the clinical assessment, conservative management, specialized diagnostic testing, and quality of life related to fecal incontinence. Methods:: Medline, PUBMED, CINAHL, and EMBASE literature databases were searched from 2016 to the end of 2020 for English language publications. Study abstracts and relevant full-text articles were retrieved and reviewed. Reference lists from articles were examined for additional studies. Recommendations for practice were made following procedures of the International Continence Society and International Consultation on Incontinence. Results:: New evidence was identified for the following topics related to FI assessment and conservative interventions: clinical assessment, patient education, diet, dietary fiber, and fluid modifications, anti-motility medications, weight loss and physical activity, PFMT, trans-anal irrigation, biofeedback, and specialized diagnostic testing as well as effects of FI on quality of life. Recommendations for practice were reviewed and updated as appropriate based on the new evidence. Conclusions:: Research examining FI assessment and conservative interventions continues to grow. Some topics in this area are understudied or in need of studies with strong, randomized, controlled designs. The results of this review serve as a summary of the state of the science and can direct future research directions.

This is the second manuscript from the Neuro-urology Promotion Committee of the International Continence Society (ICS) discussing uncommon neuro-urological conditions that are not well described in urological literature. Readers are referred to the first document for a more detailed understanding of how neurological disease might affect lower urinary tract function ( https://doi.org/10.1016/j.cont.2022.100022).Eleven conditions are covered. This includes five genetic conditions — Duchene muscular dystrophy, mitochondrial encephalopathy, Down’s syndrome, adrenoleukodystrophy and Ochoa’s syndrome. Three infection-associated conditions are covered including central nervous system tuberculosis, schistosomal myeloradiculopathy and post-polio syndrome. Three other conditions covered are myasthenia gravis, syringomyelia and the vegetative state. Key aspects and specific recommendations related to clinical practice are summarized in tables.Knowledge of unusual neurological conditions that can affect the lower urinary tract is important for ensuring a timely and precise diagnosis. This document from the ICS, along with Part I published earlier, can serve as a reference for clinicians presented with unusual forms of neurogenic lower urinary tract dysfunction.

Abstract Oxidative stress may accompany the pathological process in transient global amnesia (TGA). We measured the biological antioxidant potential (BAP) in the cerebrospinal fluid (CSF) of TGA patients. We enrolled 13 TGA patients (7 men, 6 women; mean age 65.0 years [48–70 years]) and 24 control subjects (12 men, 12 women; mean age 38.2 years [17–65 years]; age did not correlate with csfBAP in this group). We performed brain MRI in all TGA patients, and CA1 lesions were noted by MRI in 5 subjects. We measured csfBAP, total antioxidant properties, in all TGA patients and controls. csfBAP levels were higher in TGA patients than in controls (p = 0.024, 0.028). csfBAP levels in TGA patients did not differ between MRI-positive and -negative subgroups. Elevated csfBAP levels were observed in TGA patients, suggesting that oxidative stress may have a role in the pathogenesis of TGA.

It remains uncertain to what extent lower urinary tract (LUT) symptom (LUTS) is a comorbidity of myasthenia gravis (MG). We prospectively administered a LUTS questionnaire devised for detecting neurogenic pelvic organ dysfunction (not validated) in an MG group and a healthy control group and compared the results. The MG group comprised 21 patients: 15 women and 6 men, with age range 22–73 (mean 47) years, illness duration range 0.2–8 (mean 3.5) years, median Myasthenia Gravis Foundation of America (MGFA) grade 2, all walking independently. Therapies included thymectomy in 17, predonisolone 5–20 mg/day in 10, and pyridostigmine bromide 60–180 mg/day in 9 patients. The control group, who were undergoing an annual health survey, comprised 235 consecutive subjects: 120 women and 115 men, with age range 30–69 (mean 48) years. The questionnaire had 9 questions. Each question was scored from 0 (none) to 3 (severe) with an additional quality of life (QOL) index scored from 0 (satisfied) to 3 (extremely dissatisfied). Statistical analysis was made using Student’s t test. Compared with the control subjects, the frequency of LUTSs in the MG patients was significantly higher for daytime frequency (43%; p < 0.01), nocturia (24%; p < 0.01), and urinary incontinence (43%; p < 0.05). The LUTS-related QOL index for the MG patients was significantly higher for MG patients as a whole than that for all control patients (29%) (p < 0.05). In conclusion, our study results showed that MG patients had significantly more LUTSs (overactive bladder) than healthy control subjects and had worse LUTS-related QOL; therefore, amelioration of LUTS in MG is important.

It has not yet been clarified whether atherosclerotic risks other than diabetes are related to bladder small fiber neuropathy (cystopathy) in type 2 diabetes. The aim of this study was to answer this question by urodynamics. This was a retrospective study. The subjects were 44 patients: 27 male, 17 female; mean age 67.0 ± 12.7 years; mean duration of diabetes 16.8 ± 13.1 years; mean HbA1c 7.8 ± 1.2%. We analyzed the relationship between diabetic cystopathy (at least one of the following abnormalities in urodynamics: decreased bladder sensation, post-void residual, detrusor overactivity, low-compliance detrusor) and clinical items, i.e., severity and duration of diabetes, nerve conduction, body mass index, blood pressure, cardio-ankle vascular stiffness index, and ultrasound Doppler echography (plaque score, intima-media thickness) in these patients. As a result, urodynamic diabetic cystopathy was not correlated with any of the above systemic items. In conclusion, the above findings suggest that bladder small fiber neuropathy can occur independently from systemic atherosclerotic risks.

A 75-year-old Japanese man suddenly experienced right cochlear and vestibular dysfunction. Basilar artery occlusion and silent right cerebellar infarction were identified 3 days later. These were treated with intravenous ozagrel (an antiplatelet agent) and edaravone, a free-radical scavenger. The patient did not develop cerebello-brainstem signs. His first sign most probably reflected a right labyrinthine artery occlusion that heralded, or occurred together with, the basilar artery occlusion. This case highlights the possibility that a sudden inner ear dysfunction may herald a basilar stroke. Clinicians should therefore initiate appropriate therapy to prevent life-threatening brainstem complications.

We describe the case of an 86-year-old Japanese man who, by luxury perfusion after spontaneous recanalization of the left middle cerebral artery/internal carotid artery, produced acute transient sensory aphasia. This rare phenomenon is thought to be caused by reperfusion brain injury.

The management of patients with neurogenic lower urinary tract dysfunction has been well-described, however this is most frequently discussed for common conditions such as spinal cord injury or multiple sclerosis. Our objective was to review uncommon neurologic disorders and summarize both the underlying disease process, and the relevant disease-specific research on the impact of the neurologic condition on the lower urinary tract. Among the degenerative and traumatic brain disorders, we have included frontotemporal dementia, amyotrophic lateral sclerosis, Huntington’s Disease, progressive supranuclear palsy, corticobasal degeneration, multiple system atrophy, and traumatic brain injury. Among the autoimmune disorders, we reviewed transverse myelitis, neuromyelitis optica spectrum disorders, Myelin oligodendrocyte glycoprotein antibody-associated disease, glial fibrillary acidic protein astrocytopathy, and meningitis-retention syndrome (a form of aseptic meningitis that presents with urinary retention). Hereditary spastic paraplegia, VACTERL association, and several peripheral neuropathies (Guillain Barre syndrome, chronic inflammatory demyelinating polyneuropathy, autoimmune autonomic gangliopathy, Wolfram syndrome spectrum disorder (a progressive peripheral neuropathy disorder with early onset diabetes, optic atrophy and megacystis in the early stage), Charcot Marie Tooth disease, and amyloid neuropathy are included. Practice points specific to the disorders are included where appropriate.

It is not well known which of the common neuropathic distribution patterns in diabetes might suggest underlying mechanisms. To examine this question, we present data from a nerve conduction study (NCS). Irrespective of symptoms, we enrolled 323 type 2 diabetic patients (206 men, 117 women; mean age 64.1 years [51–79]; duration 12.0 years [5–19]; HbA1C 8.7% [5.1–12.1]; half [n = 142] untreated). NCS was performed for the following patterns: mononeuropathy (unilateral [MNU], bilateral [MNB]), multiple mononeuropathy (MMN), and polyneuropathy (PN). In 266 patients, we performed atherosclerosis tests: cardio-ankle vascular stiffness index (CAVI) and carotid ultrasonography. Neuropathy was observed in 235, and in 88 it was not observed; the latter then served as the control group. The most common pattern was MMN (26%), followed by MNB (18%), PN (16%), and MNU (12%). A combination of demyelination and axonal damage was revealed. Longer duration of diabetes compared with controls (8.6 years) was associated with MNB (12.5 years), MMN (14.8 years), and PN (17.4 years) (p < 0.05). HbA1C was associated with PN (p < 0.05). Atherosclerosis risks were associated with MNB, MMN, and PN (p < 0.05). Our study results indicated that (multiple) mononeuropathy is the most common distribution pattern in diabetes.

We describe the case of an 80-year-old woman with probable Creutzfeldt-Jakob disease (CJD) presenting dementia and urinary retention. Although the number of patients previously examined, including ours, is small for conclusion, provided that other etiologies of urinary retention are carefully excluded, urinary retention seems to become a feature in CJD, presumably reflecting spinal cord pathology in CJD. Physicians are advised to evaluate pelvic floor function in CJD particularly by checking post-void residuals.

We report a case of a 74-year-old Japanese woman who, after left thalamic infarction, developed right hemichorea and its neglect. This rare finding was associated with ipsi- and contralateral brain perfusion changes, presumably reflecting de-afferentiation within the brain.

We systematically reviewed literature regarding "Lewy body constipation", i.e., constipation due to Lewy body diseases (LBD), with minimal neurologic symptoms. Epidemiology and pathology studies showed that LBD can start with constipation alone, mostly due to neuronal loss and appearance of Lewy bodies in the myenteric plexus. Because LBD significantly increases with age, "Lewy body constipation" may also increase with age. Neuroimaging methods such as metaiodobenzylguanidine (MIBG) scintigraphy and dopamine transporter (DAT) scan provide a way to detect "Lewy body constipation." Key for "Lewy body constipation" includes minimal non-motor features such as REM sleep behavior disorder (night talking). Add-on therapy may be required to ameliorate constipation in patients. Diagnosis is not always easy; therefore, collaboration of gastroenterologists and neurologists is highly recommended to maximize patients' quality of life. In conclusion, "Lewy body constipation" might become a distinct category among geriatric constipation, regarding patients' follow-up and their management.

Young-onset (< 65 years) dementia is a challenging clinical problem. A 61-year-old man visited our clinic because of a 2-year history of mild cognitive impairment of the executive disorder type. He was initially suspected of having young-onset Alzheimer’s disease due to the lack of motor signs or hippocampal atrophy by conventional brain MRI. However, he proved to have anosmia, erectile dysfunction, hypersexuality, constipation, REM sleep behavior disorder, and emotional lability; imaging findings included positive brain perfusion SPECT, nigrosome MRI, DAT scan, and MIBG myocardial scintigraphy. All these clinical imaging features led to the correct diagnosis of young-onset dementia with Lewy bodies (YOD-DLB). It is hoped that this case report will help facilitate a future prospective study to diagnose and follow YOD-DLB patients with the aim of determining appropriate management and care.

AimsThe patients with Parkinson’s disease (PD) present with lower urinary tract symptoms (LUTS), but the efficacy of subthalamic nucleus deep brain stimulation (STN-DBS) on LUTS is unknown. The medial prefrontal cortex (mPFC) is a known higher micturition center which are modulated by STN-DBS. We aim to clarify STN-DBS-related changes in the neuronal activity of the mPFC in terms of bladder contraction, using normal and PD rats.MethodsExperiments in normal and 6-hydroxydopamine hemi-lesioned PD rats were conducted under urethane anesthesia. STN-DBS was applied to the left STN, with simultaneous monitoring of bladder contractions. The mPFC’s local field potential (LFP) was recorded before, during, and after STN-DBS (n = 6: normal rats, n = 6: PD rats). Before, during and after STN-DBS (n = 5: normal rats, n = 6: PD rats), extracellular fluid was collected from mPFC.ResultsSTN-DBS significantly increased bladder inter-contraction interval. STN-DBS significantly decreased mPFC alpha power in normal rat and increased alpha power in PD rat. The mPFC levels of levodopa, dopamine, serotonin and their metabolites in PD rats decreased significantly during and after STN-DBS, whereas the serotonin and its metabolites and homovanillic acid (HVA) levels decreased significantly in normal rats following STN-DBS.ConclusionSTN-DBS increased intercontraction intervals for the bladder in both normal and PD rats, as assessed by alpha power and catecholamine levels in mPFC, probably due to changes in neural activity. The effect of STN-DBS on mPFC levels of catecholamine differentiated between the normal and PD rats.

Objective Diagnosis of sporadic cerebellar ataxia is a challenge for neurologists. A wide range of potential causes exist, including chronic alcohol use, multiple system atrophy of cerebellar type (MSA-C), and sporadic late cortical cerebellar atrophy. Recently, an autosomal-dominant spinocerebellar ataxia (SCA) mutation was identified in a cohort of patients with non-MSA-C sporadic cerebellar ataxia. The aim of this study is to genetically screen genes involved in SCA in a Japanese single-hospital cohort. Methods Over an 8-year period, 140 patients with cerebellar ataxia were observed. There were 109 patients with sporadic cerebellar ataxia (no family history for at least four generations, 73 patients with MSA-C, and 36 patients with non-MSA-C sporadic cerebellar ataxia) and 31 patients with familial cerebellar ataxia. We performed gene analysis comprising SCA1, 2, 3, 6, 7, 8, 12, 17, 31, and dentatorubro-pallidoluysian atrophy (DRPLA) in 28 of 31 non-MSA-C sporadic patients who requested the test. Familial patients served as a control. Results Gene abnormalities were found in 57% of non-MSA-C sporadic cerebellar ataxia cases. Among patients with sporadic cerebellar ataxia, abnormalities in SCA6 were the most common (36%), followed by abnormalities in SCA1 (7.1%), SCA2 (3.6%), SCA3 (3.6%), SCA8 (3.6%), and DRPLA (3.6%). In contrast, gene abnormalities were found in 75% of familial cerebellar ataxia cases, with abnormalities in SCA6 being the most common (29%). For sporadic versus familial cases for those with SCA6 abnormalities, the age of onset was older (69 years vs. 59 years, respectively), and CAG repeat length was shorter (23 vs. 25, respectively) in the former than in the latter (not statistically significant). Conclusion Autosomal-dominant mutations in SCA genes, particularly in SCA6, are not rare in sporadic cerebellar ataxia. The reason for the frequency of mutations in SCA6 remains unclear; however, the reason may reflect a higher age at onset and variable penetrance of SCA6 mutations.

To determine the ability of sphincter electromyography (EMG) and post-void residual urine volume (PVR) during a free-flow study and a pressure-flow study (PFS) for distinguishing multiple system atrophy (MSA) from Parkinson's disease (PD).We retrospectively reviewed 241 case records; both urodynamic study and sphincter EMG were performed in patients with MSA (n = 147) and PD (n = 94).There was a statistically significant difference (p < 0.01) in the mean PVR during the free-flow study (113.1 ± 7.5 mL in MSA and 40.4 ± 3.8 mL in PD), mean PVR during PFS (230.1 ± 12.6 mL in MSA and 71.7 ± 6.6 mL in PD), and mean duration of MUP for sphincter EMG (9.3 ± 0.1 ms in MSA and 7.7 ± 0.1 ms in PD). The area under the curve used for differentiating MSA from PD was 0.79 and 0.73 for PVR during PFS and the free-flow study, respectively. There was a mean duration of 0.69 ms for the sphincter EMG.The present results suggested that PVR was more appropriate than sphincter EMG for differentiating MSA from PD.

It is rare that amyotrophic lateral sclerosis (ALS) presents with respiratory failure as the sole initial manifestation. A 72-year-old man with mild chronic obstructive pulmonary disease developed exertional dyspnea for 13 months. He then progressed to limb weakness that led to the diagnosis of ALS. Although rare, ALS can present with respiratory failure as the sole initial manifestation more than 1 year prior to limb weakness.

BACKGROUND:Autonomic urinary dysfunction affects patients with progressive supranuclear palsy (PSP); however, the severity and prevalence of urinary dysfunctions in these patients compared with those observed in patients with Parkinson's disease (PD) and multiple system atrophy (MSA) are unknown. OBJECTIVE:We compared urinary dysfunction characteristics in patients with PSP, PD, and MSA. PATIENTS AND METHODS:Forty-seven patients who satisfied the probable or possible criteria of the National Institute for Neurological Diseases and Stroke and Society for PSP were assessed using the urinary symptoms questionnaire and the urodynamic study at Chiba and Toho Universities (n = 26 and 21, respectively). The results were compared with those of patients with PD and MSA (n = 218 and 193, respectively). RESULTS:The mean disease duration of PSP and the mean age were 2.97 ± 0.26 and 71.4 ± 0.88 years, respectively. The mini-mental state examination and frontal assessment battery scores were 22.6 ± 0.70 and 10.7 ± 0.49, respectively. Urinary storage and voiding symptoms were observed in 57% and 56% of patients with PSP, respectively. Detrusor overactivity in the urodynamic study was detected in 81% of patients with PSP, which was slightly more than that found in patients with PD (69%) and MSA (67%); however, this was not statistically significant. Postvoid residual volume in patients with PSP was significantly more than that in patients with PD (P < 0.01), but was equivalent to that in patients with MSA. CONCLUSIONS:The present study demonstrated that patients with PSP experienced various urinary dysfunctions. Urinary storage dysfunction in patients with PSP was not different from that in patients with PD or MSA, whereas urinary voiding dysfunction in patients with PSP was milder than that in patients with MSA and more severe than that in patients with PD. These features should be taken into account for the differentiation of PSP from PD and MSA.

Positional vertigo is a common neurologic emergency and mostly the etiology is peripheral. However, central diseases may mimic peripheral positional vertigo at their initial presentation. We here describe the results of a visual suppression test in six patients with spinocerebellar ataxia type 6 (SCA6), a central positional vertigo, and nine patients with benign paroxysmal positional vertigo (BPPV), the major peripheral positional vertigo. As a result, the visual suppression value of both diseases differed significantly; e.g., 22.5% in SCA6 and 64.3% in BPPV (p < 0.001). There was a positive correlation between the visual suppression value and disease duration, cerebellar atrophy, and CAG repeat length of SCA6 but they were not statistically significant. In conclusion, the present study showed for the first time that visual suppression is impaired in SCA6, a central positional vertigo, but preserved in BPPV, the major peripheral positional vertigo, by directly comparing both groups. The abnormality in the SCA6 group presumably reflects dysfunction in the central visual fixation pathway at the cerebellar flocculus and nodulus. This simple test might aid differential diagnosis of peripheral and central positional vertigo at the earlier stage of disease.disease.

Bladder dysfunction (urinary urgency/frequency) is a common non-motor disorder in Parkinson's disease (PD). In contrast to motor disorders, bladder dysfunction is sometimes non-responsive to levodopa treatment. The brain pathology causing the bladder dysfunction (appearance of overactivity) involves an altered dopamine basal ganglia-frontal circuit, which normally suppresses the micturition reflex. The pathophysiology of the bladder dysfunction in PD differs from that in multiple system atrophy; therefore, it might aid in differential diagnosis. Anticholinergic agents are used to treat bladder dysfunction in PD, although these drugs should be used with caution particularly in elderly patients who have cognitive decline. These treatments might be beneficial in maximizing the patients' quality of life.

The cerebellum is one of the regions that contribute to urinary dysfunction in humans. A 43-year-old woman at age 35 had an acute onset of encephalitis that led to fever, generalized convulsion and coma. Six months after the disease onset, she regained consciousness and developed generalized myoclonus, cerebellar ataxia and overactive bladder, e.g., urinary urgency, daytime urinary frequency, and urinary incontinence. Eight years after the disease onset, she was revealed to have cerebellar atrophy on MRI, cerebellar hypoperfusion on SPECT, and detrusor overactivity on urodynamic study. Selective inflammation in the cerebellum seemed to produce cerebellar ataxia and overactive bladder in our case.

Isolated hemiataxia after a medullary infarct is rare. We describe a case of isolated hemiataxia after a small infarct localized at the ipsilateral dorsolateral medulla. An 83-year-old man developed acute onset of ataxia in the left arm and in both legs. Speech and extraocular movement were normal, and he did not have any other neurological manifestations. Brain MRI showed a small infarct localized at the left dorsolateral medulla, which involved the inferior cerebellar peduncle. 123ECD-SPECT showed hypoperfusion in the left cerebellar hemisphere without clear vascular territory. Neuroimaging findings for our patient suggested the involvement of the inferior cerebellar peduncle that projects to the cerebellum in our patient.

This review article introduces the new concept of vascular incontinence, a disorder of bladder control resulting from cerebral white matter disease (WMD). The concept is based on the original observation in 1999 of a correlation between the severity of leukoareosis or WMD, urinary symptoms, gait disorder and cognitive impairment. Over the last 20 years, the realization that WMD is not a benign incidental finding in the elderly has become generally accepted and several studies have pointed to an association between geriatric syndromes and this type of pathology. The main brunt of WMD is in the frontal regions, a region recognized to be crucial for bladder control. Other disorders should be excluded, both neurological and urological, such as normalpressure hydrocephalus, progressive supranuclear palsy, etc., and prostatic hyperplasia, physical stress incontinence, nocturnal polyuria, etc. Treatment involves management of small vessel disease risk factors and anticholinergic drugs that do not easily penetrate the blood brain barrier to improve bladder control.

Systemic dehydration and diffuse central nervous system signs without any other illness is referred to as dehydration encephalopathy (DE). However, the incidence of DE at emergency units remains uncertain. We investigated the incidence of DE among persons with disturbed consciousness who visited the emergency unit. We reviewed the medical case records of the emergency unit at our university hospital during a 6-month period. Among them, 132 patients presented with disturbed consciousness as the sole initial manifestation on arrival. They were 75 men, 47 women; mean age 68 years (16-95 years). After carefully excluding other etiologies, the incidence of DE was 2% among all persons in the emergency unit and 4% among persons older than 68 years.In conclusion, the incidence of DE in our emergency unit was not common. Nevertheless, recognition of DE is extremely important in order to avoid unnecessary medication in elderly subjects.

Bladder dysfunction (urinary urgency/frequency), bowel dysfunction (constipation), and sexual dysfunction (erectile dysfunction) (also called “pelvic organ” dysfunctions) are common nonmotor disorders in Parkinson's disease (PD). In contrast to motor disorders, pelvic organ autonomic dysfunctions are often nonresponsive to levodopa treatment. The brain pathology causing the bladder dysfunction (appearance of overactivity) involves an altered dopamine-basal ganglia circuit, which normally suppresses the micturition reflex. By contrast, peripheral myenteric pathology causing slowed colonic transit (loss of rectal contractions) and central pathology causing weak strain and paradoxical anal sphincter contraction on defecation (PSD, also called as anismus) are responsible for the bowel dysfunction. In addition, hypothalamic dysfunction is mostly responsible for the sexual dysfunction (decrease in libido and erection) in PD, via altered dopamine-oxytocin pathways, which normally promote libido and erection. The pathophysiology of the pelvic organ dysfunction in PD differs from that in multiple system atrophy; therefore, it might aid in differential diagnosis. Anticholinergic agents are used to treat bladder dysfunction in PD, although these drugs should be used with caution particularly in elderly patients who have cognitive decline. Dietary fibers, laxatives, and “prokinetic” drugs such as serotonergic agonists are used to treat bowel dysfunction in PD. Phosphodiesterase inhibitors are used to treat sexual dysfunction in PD. These treatments might be beneficial in maximizing the patients' quality of life.

Although the hippocampus has not typically been identified as part of the language and aphasia circuit, recent evidence suggests that the hippocampus is closely related to naming, word priming, and anomic aphasia. A 59-year old woman with limbic encephalitis of possible autoimmune etiology, after recovery of consciousness, presented with severe memory impairment in both anterograde and retrograde modalities, episodes of fear, hallucination and convulsion, and transient fluent, phonemic paraphasia, together with small sharp waves diffusely by EEG. Brain MRI revealed bilateral symmetric, discrete lesions in the body to the infundibulum of the hippocampus. The transient phonemic paraphasia noted in our patient may have been a result of primary damage in the hippocampus and its fiber connection to the Wernicke’s area or secondary partial status epilepticus that might have originated in the hippocampus.