Background Lyme disease (LD) is an infectious multi-system illness caused by the bacterial genus Borrelia and spread by bites of infected ticks. Although most patients are successfully treated by timely antibiotic therapy, it is broadly accepted that a sizeable number of patients experience treatment failure and continue to suffer long-term, debilitating symptoms, including pain, fatigue, cognitive dysfunction and other symptoms. This is known as post-treatment LD (PTLD), for which diagnosis is not standardized and treatment remains controversial. The prevalence and societal burden of PTLD is unknown. Methods In an effort to help characterize the LD landscape, we estimated the number of PTLD cases in the US in 2016 and 2020 using Monte-Carlo simulation techniques, publically-available demographic datasets, uncertainty in the inputs and realistic assumptions about incidence and treatment failure rates. Results Depending on the input assumptions, PTLD prevalence estimates for 2016 ranged from 69,011 persons (95% CI 51,796 to 89,312) to 1,523,869 (CI 1,268,634 to 1,809,416). Prevalence in 2020 is predicted to be higher than 2016, and may be as high as 1,944,189 (CI 1,619,988 to 2,304,147) cases. Conclusions The cumulative prevalence of PLTD in the United States is estimated to be high and continues to increase. These findings will be of interest to epidemiologists and health economists studying disease burden in the US and elsewhere, and justify funding to study PTLD diagnosis and treatment.

In a retrospective study of 84 outpatients with multiinfarct dementia, urinary and gait disturbances were found in 50% and 27%, respectively, and often preceded dementia and discrete stroke-like episodes by more than 5 years. Compared to patients without urinary disturbance, those with urinary dysfunction were predominantly male and more behaviorally impaired, but were similar in age, cognitive score, depression score, computerized tomography findings, and relative survival. Compared to patients without gait disturbance, those with gait abnormality had a higher Hachinski iscbemic score and depression score and were more behaviorally impaired. Urinary and gait abnormalities may be markers for cerebrovascular disease and vascular dementia even in the absence of frank stroke. Damage to bifrontal outflow tracts may be the common pathophysiological mechanism underlying the behavioral and motor symptoms characteristic of vascular dementias. 4 There is presently no accepted treatment for this disease, but there is some rationale for the prevention of MID via the control of risk factors for stroke and by the prophylactic administration of aspirin to patients at risk. Identification of clinical markers for early MID might allow early recognition of highrisk groups so that prophylactic treatment might prevent or delay the development of this fulminant disorder.We therefore examined the prevalence of various risk factors for stroke and vascular disease in our patients with clinical MID. Patients with MID may have a long history of gait or urinary disturbances preceding overt dementia and discrete cerebrovascular events, and we sought to investigate this relation in a retrospective series. Subjects and MethodsThe Geriatric Evaluation Service at The Burke Rehabilitation Center in White Plains, New York, is an outpatient dementia clinic that has studied more than 700 patients over the last 6 years, as described previously.3 All patients had a complete medical, neurological, psychiatric, and neuropsychological evaluation, with laboratory work, brain computerized tomography (CT), and EEG to rule out treatable causes and a modified Hachinski score 6 of 2 6. Patients thought to have a mixed dementia or a multiinfarct state coexistent with Alzheimer's disease were excluded, as were patients with dementias of other etiologies such as head trauma, alcohol abuse, or metabolic encephalopathies. Each patient's record was reviewed for 1) risk factors for and manifestations of vascular disease, 2) family history of hypertension, diabetes mellitus, coronary artery disease, myocardial infarction, and cerebrovascular accident, 3) manifestations of cerebrovascular disease such as stroke, carotid disease or surgery, and transient ischemic attacks (TIA's), 4) neurologic history and examination, 5) scores for ischemic dementia (modified Hachinski score 6 ), cognitive impairment ("mental status quotient" 7 ), behavioral impairment (Haycox score 8 ), and depression (Hamilton score), and 6) brain CT findings.Subgroups with urinary and/or gait dis...

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We examined 75 consecutive patients with closed head trauma and found that 15 (20%) had moderate to severe gait ataxia (GA) 1-8 months after injury. Evaluation over 4 years revealed that the GA improved in six patients, and was persistent in nine others. All patients with chronic GA also displayed ocular motor abnormalities and/or large amplitude intention tremor when first and later examined. Those in whom GA disappeared never displayed eye movement abnormalities or tremor. The findings suggest that ocular motor abnormalities and/or intention tremor are poor prognostic signs for recovery from posttraumatic gait ataxia, and that posttraumatic gait ataxia without associated ocular motor or cerebellar tract injury has a better prognosis and might eventually disappear.The data suggest that damage to cerebellar outflow tracts, ocular motor nuclei, or fascicles may be irreversible whereas intrinsic cerebellar injury might be reversible.