The present study was undertaken to investigate the effect of prenatal protein deprivation on the postnatal development of the mossy fiber plexus of the hippocampal formation on postnatal (P) days 15, 30, 90, and 220. Although there is extensive information about the effects of malnutrition on cell body and dendrite morphology, little attention has been paid to axons or axon plexuses. The mossy fiber plexus represents the dentate gyrus granule cell axonal projection to areas CA4 and CA3 of the hippocampal formation and is readily demonstrated with Timm's heavy metal stain. With the use of this stain, the plexus was measured at 13 levels throughout the hippocampal complex. There was no effect of the diet on the anatomical distribution of the plexus. The current study, however, does show significant effects of prenatal protein malnutrition on postnatal development of the mossy fiber plexus that are age dependent. The prenatally malnourished rats show significant deficits in the total rostro-caudal extent and volume of the plexus on P15, P90, and P220, with the most marked dietary effect on P220. There was no significant diet effect on P30 in either extent or volume.

The present study was undertaken to investigate the effect of prenatal protein deprivation on area CA1 hippocampal pyramidal cells on postnatal (P) days 15, 30, 90 and 220 using Golgi techniques. Age related changes in both groups and diet related changes between groups were assessed. There were significant diet effects at all four ages, with one of 12 different measurements showing a significant diet effect on P15, five on P30, one on P90, and seven on P220. The most marked effect of the diet was on pyramidal cell dendrite spine density in the stratum moleculare and stratum radiatum, with a different pattern of diet effects in the two strata. In pyramidal cell dendrites in the stratum moleculare, there was a deficit in spine density that was significant at three of the four ages and there were similar age-related changes in the two diet groups. Spines on pyramidal cell dendrites in the stratum radiatum showed a lack of synchrony of age-related changes in the two diet groups, with an increased spine density in the malnourished rats on P30 and a widening deficit in this parameter on P90 and P220. The bimodal distribution to these changes, with most marked deficits occurring on P30 and P220, with an intervening period of apparent “catch-up” on P90, is of interest and may be a significant brain adaptation to malnutrition. The present study is the final of three morphometric studies on the effect of prenatal protein restriction on three key neurons in the hippocampal trisynaptic circuit. When compared to our previous studies on the dentate granule cell and the CA3 pyramidal cell, it is noted that there is an effect of the low protein diet on all these neurons, with the most marked effect on the predominantly postnatally generated dentate granule cells. Hippocampus 7:192–203, 1997. © 1997 Wiley-Liss, Inc.

The present study was undertaken to investigate the effect of prenatal protein deprivation on the postnatal development of the mossy fiber plexus of the hippocampal formation on postnatal (P) days 15, 30, 90, and 220. Although there is extensive information about the effects of malnutrition on cell body and dendrite morphology, little attention has been paid to axons or axon plexuses. The mossy fiber plexus represents the dentate gyrus granule cell axonal projection to areas CA4 and CA3 of the hippocampal formation and is readily demonstrated with Timm's heavy metal stain. With the use of this stain, the plexus was measured at 13 levels throughout the hippocampal complex. There was no effect of the diet on the anatomical distribution of the plexus. The current study, however, does show significant effects of prenatal protein malnutrition on postnatal development of the mossy fiber plexus that are age dependent. The prenatally malnourished rats show significant deficits in the total rostro-caudal extent and volume of the plexus on P15, P90, and P220, with the most marked dietary effect on P220. There was no significant diet effect on P30 in either extent or volume. Hippocampus 7:184–191, 1997. © 1997 Wiley-Liss, Inc.

The present study was undertaken to investigate the effect of prenatal protein deprivation on area CA1 hippocampal pyramidal cells on postnatal (P) days 15, 30, 90 and 220 using Golgi techniques. Age related changes in both groups and diet related changes between groups were assessed. There were significant diet effects at all four ages, with one of 12 different measurements showing a significant diet effect on P15, five on P30, one on P90, and seven on P220. The most marked effect of the diet was on pyramidal cell dendrite spine density in the stratum moleculare and stratum radiatum, with a different pattern of diet effects in the two strata. In pyramidal cell dendrites in the stratum moleculare, there was a deficit in spine density that was significant at three of the four ages and there were similar age-related changes in the two diet groups. Spines on pyramidal cell dendrites in the stratum radiatum showed a lack of synchrony of age-related changes in the two diet groups, with an increased spine density in the malnourished rats on P30 and a widening deficit in this parameter on P90 and P220. The bimodal distribution to these changes, with most marked deficits occurring on P30 and P220, with an intervening period of apparent "catch-up" on P90, is of interest and may be a significant brain adaptation to malnutrition. The present study is the final of three morphometric studies on the effect of prenatal protein restriction on three key neurons in the hippocampal trisynaptic circuit. When compared to our previous studies on the dentate granule cell and the CA3 pyramidal cell, it is noted that there is an effect of the low protein diet on all these neurons, with the most marked effect on the predominantly postnatally generated dentate granule cells.

A review of the neuropathology of infantile autism shows abnormalities in the limbic forebrain and in cerebellar circuits. The role of the cerebellar lesions in the symptomatology of infantile autism is unknown. The cerebellar findings appear to date from a fetal stage of development with evidence for an ongoing process after birth. The timing of the findings in the limbic system is unknown. A postulated role for these findings in the limbic system in infantile autism is presented.

A 23-year-old man injured his foot in a motorcycle accident. Roentgenograms and computed tomography scans demonstrated a Hawkins Type III fracture-dislocation of the talus with a suspected disruption of the anterior tibiofibular ligament. Prompt anatomic reduction of the talus with rigid internal fixation was performed. Intraoperative stress roentgenograms confirmed the presence of a syndesmotic disruption. No cases of this injury have been reported in the literature. When no obvious fracture of the ankle mortise is present in a Hawkins Type III or IV talar fracture-dislocation, care must be taken to fully evaluate the osseous and ligamentous structures of the ankle to rule out an occult injury. Computed tomography scans, stress roentgenograms, intraoperative clinical examination, and direct visual inspection can all be used to aid in this evaluation.

Destruction of the calcaneal fat pad has been implicated as a source of chronic pain following fractures of the os calcis. Several investigators postulate that the initial trauma that produces a calcaneal fracture also results in destruction of the U-shaped fibrous septa that maintain the piston-like organization of the fat columns. Fibrosis and loss of the protective cushioning provided by the fat pad may eventually occur. The authors report on the largest series of magnetic resonance images of the calcaneal fat pad in the heels of patients with calcaneal fractures. A prospective consecutive study utilizing magnetic resonance imaging was performed on 22 heels with calcaneal fractures. Ten contralateral heels without calcaneal fracture and the heels of five normal subjects were scanned as controls. No signal changes suggestive of increased fat pad edema, fibrosis, or fatty release were detected. In addition, the vertical septa were well visualized and found to be intact in all cases. The height of the fat pad was measured, with no changes noted as compared with the contralateral heel. In those patients with acute fractures, signal changes suggestive of hematoma were well visualized in the soft tissue surrounding the calcaneus. In two of these cases, there was extension beneath the plantar fascia, but no penetration into the fat columns. Magnetic resonance imaging allows excellent detailed visualization of the calcaneal fat pad and surrounding structures. No evidence is found to support the hypothesis that marked damage to the gross structure of the fat pad occurs at the time of injury.(ABSTRACT TRUNCATED AT 250 WORDS)

A child was brought for evaluation of signs of unilateral chronic progressive sciatic nerve dysfunction found to be due to nerve entrapment in the thigh by a fibrovascular band. Sectioning of the band was followed by marked improvement in the nerve function. Compression by a band is a rare but treatable cause of sciatic neuropathy.