Article abstract—Objective: To update the 1994 practice parameter for the diagnosis of dementia in the elderly. Background: The AAN previously published a practice parameter on dementia in 1994. New research and clinical developments warrant an update of some aspects of diagnosis. Methods: Studies published in English from 1985 through 1999 were identified that addressed four questions: 1) Are the current criteria for the diagnosis of dementia reliable? 2) Are the current diagnostic criteria able to establish a diagnosis for the prevalent dementias in the elderly? 3) Do laboratory tests improve the accuracy of the clinical diagnosis of dementing illness? 4) What comorbidities should be evaluated in elderly patients undergoing an initial assessment for dementia? Recommendations: Based on evidence in the literature, the following recommendations are made. 1) The DSM-III-R definition of dementia is reliable and should be used (Guideline). 2) The National Institute of Neurologic, Communicative Disorders and Stroke‐AD and Related Disorders Association (NINCDS-ADRDA) or the Diagnostic and Statistical Manual, 3rd edition, revised (DSM-IIIR) diagnostic criteria for AD and clinical criteria for Creutzfeldt‐Jakob disease (CJD) have sufficient reliability and validity and should be used (Guideline). Diagnostic criteria for vascular dementia, dementia with Lewy bodies, and frontotemporal dementia may be of use in clinical practice (Option) but have imperfect reliability and validity. 3) Structural neuroimaging with either a noncontrast CT or MR scan in the initial evaluation of patients with dementia is appropriate. Because of insufficient data on validity, no other imaging procedure is recommended (Guideline). There are currently no genetic markers recommended for routine diagnostic purposes (Guideline). The CSF 14-3-3 protein is useful for confirming or rejecting the diagnosis of CJD (Guideline). 4) Screening for depression, B12 deficiency, and hypothyroidism should be performed (Guideline). Screening for syphilis in patients with dementia is not justified unless clinical suspicion for neurosyphilis is present (Guideline). Conclusions: Diagnostic criteria for dementia have improved since the 1994 practice parameter. Further research is needed to improve clinical definitions of dementia and its subtypes, as well as to determine the utility of various instruments of neuroimaging, biomarkers, and genetic testing in increasing diagnostic accuracy.

https://n.neurology.org/content/neurology/56/9/1143.full.pdf

Practice parameter: Diagnosis of dementia (an evidence-based review) Report of the Quality Standards Subcommittee of the American Academy of Neurology

ALS: a disease of motor neurons and their nonneuronal neighbors.

The neuropsychopharmacology of phencyclidine: from NMDA receptor hypofunction to the dopamine hypothesis of schizophrenia.

Nerve regeneration is a complex biological phenomenon. In the peripheral nervous system, nerves can regenerate on their own if injuries are small. Larger injuries must be surgically treated, typically with nerve grafts harvested from elsewhere in the body. Spinal cord injury is more complicated, as there are factors in the body that inhibit repair. Unfortunately, a solution to completely repair spinal cord injury has not been found. Thus, bioengineering strategies for the peripheral nervous system are focused on alternatives to the nerve graft, whereas efforts for spinal cord injury are focused on creating a permissive environment for regeneration. Fortunately, recent advances in neuroscience, cell culture, genetic techniques, and biomaterials provide optimism for new treatments for nerve injuries. This article reviews the nervous system physiology, the factors that are critical for nerve repair, and the current approaches that are being explored to aid peripheral nerve regeneration and spinal cord repair.

Neural tissue engineering: strategies for repair and regeneration.

Cardiovascular toxicity and titin cross-reactivity of affinity-enhanced T cells in myeloma and melanoma

Spontaneous paroxysmal electroclinical patterns in rat: A model of generalized non-convulsive epilepsy

Summary: Of 100 randomly chosen, adult male Wistar rats in the breeding colony at the Centre de Neurochimie, Strasbourg, 31 presented spontaneous, nonconvulsive epileptic seizures: wave-and-spike discharges, 7–11 cy-cles/s, 200–600 μV, accompanied by behavioral arrest and myoclony of the vibrissae and of the facial and cervical muscles. Pentylenetetrazol (PTZ) 10 and 20 mg/kg increased the duration and number of seizures by 100–150% in these spontaneously epileptic animals, and caused identical seizures in apparently normal rats. Sodium valproate, diazepam, trimethadione, and ethosux-imide suppressed the spontaneous seizures and protected against PTZ-induced seizures in a dose-dependent fashion. Carbamazepine and diphenylhydantoin were inefficacious or aggravative in the two cases. The clinical, EEG, and pharmacological observations suggest that the Wistar rats displaying spontaneous seizures constitute a valid physiological and pharmacological model of petit mal absences, presenting advantages compared to the usual models in which seizures are induced byinjected epileptogenic drugs.



RESUME

Sur 100 rats Wistar, mâles, adultes, preleves au hasard dans Ľe1evage du Centre de Neurochimie de Strasbourg, 31 ont presente spontanement des crises epileptiques nonconvulsives (de-charges de pointes-ondes de 7–11 c/s et de 200–600 μ V accom-pagnees ďun arret de Ľactivite et de myoclonies des vibrisses et de la musculature faciale et cervicale). Le pentylenetetrazol a 10 et 20 mg/kg augmente de 100–150% la duree et le nombre des crises chez les animaux spontanement epileptiques; aux memes doses, le pentylenetetrazol fait apparaitre des crises iden-tiques chez les animaux apparemment indemnes. Le valproate de sodium, le diazepam, la trimethadione, et Ľethosuximide sup-priment les crises spontanees et protegent contre les crises induces par 20 mg/kg de PTZ de facon dose-dependante. La car-bamazepine et la diphenylhydantoine sont inefficaces ou aggravates sur les deux types de crises. Ľensemble des resultats cliniques, electroencephalographiques, et pharmacologiques permettent de penser que les crises spontanees du rat Wistar constituent un bon modele physiologique et pharmacologique ďabsences. Ce modele semble presenter quelques avantages par rapport aux modeles usuels induits par des injections de drogues epileptogenes.



RESUMEN

De las 100 ratas Wistar machos y adultos, seleccionadas al azar de la colonia de crias del Centro de Neuroqui'mica en Es-trasburgo, 31 presentaron ataques epilepticos no convulsivos: descargas punta-onda de 7 a 11 ciclos por segundo y 200 a 600 μ.V, acompanadas de interrupcion del comportamiento y mio-clonias de las vibrisas y de los musculos faciales y cervicales. La administracion de 10 a 20 mg/kg de pentilentetrazol (PTZ) incrementaron en un 100 a 150% la duracion y el numero de los ataques en estos animales espontaneamente epilepticos y causo ataques identicos en ratas aparentemente normales. El valproato sodico, el diazepan, la trimetadiona y la etosuximida suprimieron los ataques espontaneos y protegieron a las ratas de las crisis inducidas por el PTZ. La carbamazepina y la difenilhidantoina fueron ineficaces o perjudiciales en dos casos. Las observa-ciones clinicas, electroencefalograficas y farmacologicas sugi-eren que las ratas Wistar que muestran ataques espontaneos con-stituyen un valido modelo fisiologico y farmacologico de las au-sencias petit-mal. Este modelo presenta ventajas con respecto a modelos comunes en los que los ataques se inducen inyectando drogas epileptogenicas.



ZUSAMMENFASSUNG

Von 100 zufallig ausgewahlten mannlichen erwachsenen Wistar-Ratten aus der Zuchtkolonie am Centre de Neurochimie, Strasburg zeigten 31 spontane, nicht konvulsive epileptische Anfalle: wave and spike Entladungen von 7 bis 11 c/s und 200 bis 600 uV, die von einem Verharren und Myokloni der Schnau-zhaare sowie der facialen und cervikalen Muskeln begleitet waren. Pentylentetrazol (PTZ) in einer Dosis von 10 und 20 mg/ kg verlangerte bei diesen spontan epileptischen Tieren die Dauer und erhohte die Anzahl der Anfalle um 100 bis 150%. Daruber hinaus verursachte diese Dosis identische Anfalle bei scheinbar normalen Ratten. Natrium Valproat, Diazepam, Trimethadion und Ethosuximid unterdruckten die spontanen Anfalle und schutzten, in Abhangigkeit von der Dosis, vor PTZ-induzierten Anfallen. Carbamazepin und Diphenylhydantoin waren wir-kungslos; in 2 Fallen verstarkten sie die Anfalle. Die klinischen, EEG, und pharmakologischen Beobachtungen legen nahe, daβ die Wistar-Ratten mit spontanen Anfallen ein gutes physiolo-gisches und pharmakologisches Modell der Petit Mai Absencen darstellen, das Vorteile gegenuber den ubrigen Modellen bietet, bei denen epileptogene Medikamente injiziert werden mussen.

Jean-Marie Warter

Papers

Spontaneous paroxysmal electroclinical patterns in rat: A model of generalized non-convulsive epilepsy

A Model of Chronic Spontaneous Petit Mal‐like Seizures in the Rat: Comparison with Pentylenetetrazol‐Induced Seizures

Spontaneous spike and wave discharges in thalamus and cortex in a rat model of genetic petit mal-like seizures

Enhancement of spike and wave discharges by GABAmimetic drugs in rats with spontaneous petit-mallike epilepsy

Kindling of audiogenic seizures in Wistar rats: An EEG study