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Hyperglycemia of diabetes mellitus causes damage at the vascular level, which at the renal level represents diabetic nephropathy. In this pathology, there is arterial hypertension. In addition, several reports suggest that hyperglycemia and arterial hypertension affect interneuronal communication at the level of dendritic morphology. We studied these changes in an animal model with streptozotocin-induced diabetes mellitus in the spontaneous hypertensive (SH) rat. Recent reports from our laboratory have demonstrated that cerebrolysin (CBL), a preparation of neuropeptides with protective and repairing properties, reduces dendritic deterioration in both pathologies, in separate studies. In the present study, we evaluated the effect of CBL using the animal model with hyperglycemia and arterial hypertension and assessed the dendritic morphology using a Golgi-Cox staining procedure. Our results suggest that CBL ameliorated the reduction in the number of dendritic spines in the PFC and hippocampus caused by hyperglycemia in the SH rat. In addition, CBL also increased distal dendritic length in the PFC and hippocampus in hyperglycemic SH rats. Consequently, the CBL could be a therapeutic tool used to reduce the damage at the level of dendritic communication present in both pathologies.

Converging evidence suggests that human aging is associated with structural, functional, and cognitive deteriorations that preferentially affect the frontal lobe of the brain. Because a decline in frontal cognitive functions may be associated with subsequent declines in global cognitive function and functional activities, interventions that effectively enhance frontal lobe functions of older adults are clinically important. In this chapter, we propose that photobiomodulation (PBM) can be an effective treatment option to protect the aging neurons and enhance frontal lobe functions in normal older adults. Specifically, aging is associated with frontal hypometabolism; through its effects on mitochondrial functioning, PBM may increase energy production and oxygen supply to support metabolism of the aging neurons. In addition, aging is associated with neural atrophy and loss of synapses; through its effects on transcription factors, PBM may promote neuronal survival and encourage the formation of new cells and synapses in the aging frontal cortex.

Importance Macular telangiectasia type 2 is a bilateral disease with characteristic alterations of the macular capillary network and neural atrophy. Vascular and neurodegenerative hypotheses have been proposed to explain these clinical findings, but many questions regarding the pathogenesis remain. Observations We report the case of a 69-year-old woman with macular telangiectasia type 2 in whom multimodal fundus imaging identified neuronal features without clinically detectable vasculopathy. Conclusions and Relevance We hypothesize that parallel neuronal and vascular pathogenic pathways secondary to Muller cell dysfunction, the cause of which remains obscure, explain the clinical features of this case of macular telangiectasia type 2.

Pyruvate kinase activity was examined in the sera of a group of patients with neuromuscular disease and in carriers, and compared with that of creatine kinase. The following observations were made: 1. 1. Pyruvate kinase activity was elevated in all 14 patients with Duchenne muscular dystrophy, with very high values generally correlating inversely with age or disease duration. Elevated values of pyruvate kinase were usually, but not invariably, associated with elevated values of creatine kinase. 2. 2. Almost all patients with other muscle diseases and those with neural atrophy had modest elevations in pyruvate kinase activity. 3. 3. Ten of 17 individuals were identified as carriers of muscle disease by using both pyruvate kinase and creatine kinase while eight and nine, respectively, were detected using either assay alone. 4. 4. When frozen stored EDTA-plasma was used for pyruvate kinase estimation, higher levels, as compared with the corresponding sera or fresh plasma, were found in controls and carriers but not in Duchenne muscular dystrophy patients. Frozen stored EDTA-plasma should, therefore, not be used for diagnostic purposes.

The effects of time-expanded monosyllabic words (NU-6) on the auditory discrimination performance of 15 young adults with normal hearing and 20 elderly subjects were studied. Three conditions of time expansion, 30, 60 and 100%, plus a 0% control condition, were presented at four sensation levels (8, 16, 24 and 32 dB). For the normally hearing subjects, auditory discrimination performance at all ratios of time expansion was equal to the 0% condition. Results for the elderly subjects indicated intelligibility was inversely related to time expansion at the 30 and 60% conditions. However, at the 100% condition, speech intelligibility improved over the 60% condition at 8 and 16 dB sensation level. At 24 and 32 dB sensation level, performance at 100% was equal to the 60% condition. With the normal and elderly subjects, ear and list effects were minimal. The results are discussed in terms of the clinical value of this procedure and in light of literature that reviews the performance of subjects on tests employing various temporally altered stimuli.

The authors describe a case of scapulo-tibio-peroneal amyotrophy of early onset. The spinal nature of the disease is indicated by the electromyographic and histoenzymologic evidence. Two brothers of the patient show a distal muscular wasting in the lower limbs. The nosographic position and the possible relationship of this form with the neural atrophy of Charcot-Marie-Tooth are discussed.

The clinical history, examination and treatment of a case of cranial myodegeneration are described. Observations extended over a period of 3 years, 8 months, and during this period three biopsies were taken from the muscles of mastication (temporal and masseter muscles). The results of the post-mortem examination are also recorded. The histological changes in the muscles of mastication were consistent with a diagnosis of neural atrophy, but it was not possible to confirm this by histological examination of the central nervous system. The differential diagnosis of cranial myodegeneration is discussed. Resume. On decrit le developpement clinique, l'examen et le traitement d'un cas de degene-rescence musculaire crânienne. Les observations se sont deroulees sur une periode de trois ans huit mois et au cours de cette periode, on a fait trois biopsies des muscles de mastication (muscles temporal et masseter). On donne egalement les resultats de l'autopsie. Les modifications histologiques observees dans les muscles de mastication donnaient appui au diagnostic d'atrophie neurale, mais il n'etait pas possible de le confirmer par un examen histologique du systeme nerveux central. On examine le diagnostic differentiel de la degenerescence musculaire crânienne. Zusammenfassung. Die klinische Geschichte, Untersuchung und Behandlung eines Falles von cranialer Myodegeneratio werden beschrieben, Die Beobachtungen erstreckten sich uber drei Jahre und acht Monate, und wahrend dieser Periode wurden drei Biopsien an den Kaumuskeln (Temporal- und Massetermuskeln) vorgenommen. Die Ergebnisse der Sektion wurden ebenfalls festgehalten. Die histologischen Veranderungen in den Kaumuskeln stimmten mit einer Diagnose auf neurale Atrophie uberein, aber es war nicht moglich, dies mit einer histologischen Untersuchung des Zentralnervensystems zu bestatigen. Die Differentialdiagnose der cranialen Myodegeneratio wird besprochen.

A study of the maximum and minimum motor conduction velocity by techniques for measuring the dispersion (Hopf, desynchronisation) was made in clinical cases of Charcot-Marie-Tooth-Hoffmann disease and in their healthy relatives, and in cases of Steinert's syndrome. It revealed an initial elective involvement of the fibers with a higher motor conduction velocity and only secondarily (in the more advanced cases of C.M.T.H.) involvement of the slower conducting fibers, both in distal neural atrophy and in Steinert's syndrome. The data are discussed in the light of current thinking on the neurophysiology and histoenzymology of motor unit impairment in these two diseases.

To the Editor.— The articles of Duncan et al 1 and Izumi 2 on generalized perforating granuloma annulare prompted us to report a case of ours. Report of a Case.— A 42-year-old woman was referred to the Department of Dermatology, Wroclaw School of Medicine, Poland in June 1971 for evaluation of gradually progressive papular lesions scattered over the extremities, trunk, and face. The asymptomatic skin lesions had been first noticed about one year ago. The family history was negative for skin diseases. The patient had a 15-year history of progressive neural atrophy. Physical examination revealed a diffuse eruption of more than 500 papules, involving most areas of skin, except for the palms, with maximum involvement of face, extensor aspects of extremities, interscapular region, soles, and pinnae of the ears. The majority of the lesions were 3 to 5 mm erythematous papules. Individual papules developed a central umbilication, then the center