Anterior Parahippocampal Gyrus Research Articles

The functional anatomy of imagining and perceiving colour.

We report two functional magnetic resonance imaging experiments which reveal similarities and differences between perceptual and imaginal networks within the single visual submodality of colour. The first experiment contrasted viewing of a coloured and grey-scale Mondrian display, while the second contrasted a relative colour judgement with a spatial task and required the generation of mental images. Our results show that colour perception activates the posterior fusiform gyrus bilaterally (area V4), plus right-sided anterior fusiform and lingual gyri, striate cortex (area V1), and the left and right insula. Colour imagery activated right anterior fusiform gyrus, left insula, right hippocampus and parahippocampal gyrus, but not V4 or V1. The findings reconcile neurological case studies suggesting a double dissociation between deficits in colour imagery and perception and point to anterior fusiform, parahippocampal gyri and hippocampus as the location for stored representations of coloured objects.

Volumes of Medial Temporal Lobe Structures in Patients with Alzheimer’s Disease and Mild Cognitive Impairment (and in Healthy Controls)

Background: The clinical diagnosis of Alzheimer’s disease (AD) can be difficult to make in early stages of disease. Structural neuroimaging offers a potential tool in the clinical diagnosis of AD with mild cognitive impairment. Postmortem studies indicate that early neuropathology in AD occurs in medial temporal lobe limbic structures. Magnetic resonance imaging (MRI) studies that assessed these volumes in mildly impaired AD patients remain inconclusive. Methods: Using MRI, we measured volumes of left and right hippocampus, amygdala, and anterior and posterior parahippocampal gyrus (PHG) in 13 AD patients with mild cognitive impairment, defined as ≥ 20 on the Mini-Mental State Exam, and in 21 healthy age- and sex-matched controls. Results: The AD patients had smaller medial temporal lobe volumes, except for the right anterior PHG. Discriminant function analysis using MRI volumes produced 94% correct group classification. Conclusions: These results show that in mildly impaired A%D patients atrophy is present in medial temporal lobe structures; that MRI volumes of the anterior PHG, which contains entorhinal cortex, are reduced, but the amygdala and hippocampal volumes show greater reduction; and that discriminant function analysis using all volumes as predictors can correctly classify a high proportion of individuals.

Subtemporal transparahippocampal amygdalohippocampectomy for surgical treatment of mesial temporal lobe epilepsy. Technical note.

Amygdalohippocampectomy (AH) is an accepted surgical option for treatment of medically refractory mesial temporal lobe epilepsy. Operative approaches to the amygdala and hippocampus that previously have been reported include: the sylvian fissure, the superior temporal sulcus, the middle temporal gyrus, and the fusiform gyrus. Regardless of the approach, AH permits not only extirpation of an epileptogenic focus in the amygdala and anterior hippocampus, but interruption of pathways of seizure spread via the entorhinal cortex and the parahippocampal gyrus. The authors report a modification of a surgical technique for AH via the parahippocampal gyrus, in which excision is limited to the anterior hippocampus, amygdala and parahippocampal gyrus while preserving the fusiform gyrus and the rest of the temporal lobe. Because transparahippocampal AH avoids injury to the fusiform gyrus and the lateral temporal lobe, it can be performed without intracarotid sodium amobarbital testing of language dominance and language mapping. Thus the operation would be particularly suitable for pediatric patients in whom intraoperative language mapping before resection is difficult.

A new trend in operative technique for intracerebral hemorrhage: a comparative study of stereotactic endoscopic removal and stereotactic catheter drainage.

The development of less invasive methods to evacuate intracerebral hematomas (ICHs) has improved outcome in patients with traumatic brain injury. Eighteen patients with ICHs underwent surgery via one of two methods: stereotactic endoscopic removal (SER) or stereotactic catheter drainage (SCD). The outcome results were then compared. The patient population was composed of 11 men and seven women with a mean age of 53.3 years (range 33-81 years), all suffering from ICH in the basal ganglia. The mean hematoma volume was 34.4 ml (range 23-105 ml). All patients had major neurological deficits, but showed no sign of transtentorial herniation. Ten patients underwent SCD and eight had SER. All procedures were performed within 24 hours of insult. After local anesthesia was induced in the patient, an intracranial pressure (ICP) monitoring catheter and an Otzuki cannula were placed through separate burr holes in the skull. Using the SER technique, the ICH was removed using suction and forceps through the side window of the cannula until the ICP had decreased significantly. Hemostasis was attained by lesioning with a Nd-YAG laser. In the SCD procedure, we placed a silicone catheter into the hematoma to drain it and then added urokinase. The hematoma was drained for 3 to 5 days in the SER method and 7 to 10 days in the SCD method. Rebleeding occurred in one of the early cases in which we used the SER procedure. At follow-up evaluation, the mortality rate was 13% in the SER group and 10% in the SCD group. The patients in whom outcome was most improved from these treatments were those who had been admitted with an impaired level of consciousness. Stereotactic catheter drainage is a precise, safe, and brief procedure with a very low rebleeding rate, but its outcome effect was more delayed than other procedures. Stereotactic endoscopic removal can easily replace SCD, with a similar mortality rate. Both procedures can be accomplished under direct visualization so as to eliminate any undesirable event or outcome.

Involvement of the amygdala, dentate and hippocampus in motor neuron disease

A pathological hallmark of motor neuron disease (MND) is the presence of ubiquitinated inclusions in lower motor neurons. Recently, ubiquitin-immunoreactive inclusions have been found in neocortical and hippocampal neurons, indicating that in some cases there may be extensive extra-motor involvement. We have observed that some cases of MND with dementia (MND-D), had ubiquitinated inclusions in the amygdala. In order to study this systematically, we examined 18 cases of ‘typical’ MND, 4 cases of MND-D and 12 neurologically normal and abnormal controls, using antibodies against ubiquitin and a range of cytoskeletal proteins. In addition to standard neuropathological examination, we examined in detail the anterior thalamus, parahippocampal gyrus, dentate gyrus of the hippocampus, and the amygdala. We found ubiquitin immunoreactive inclusions in the amygdala and parahippocampal gyrus in more than 30% of MND cases, most of whom were not known to have significant cognitive impairment. These inclusions did not react with antibodies against tau or with phosphorylated neurofilaments. They thus differ from the inclusions of Alzheimer's disease, and they do not have the appearance or immunocytochemical features of cortical Lewy bodies. In parallel studies we have found selective cognitive impairments in about 25% of our patients with typical MND, and PET activation studies show impaired activation in the anterior thalamus, parahippocampal gyrus and medial frontal regions. Since the amygdala is an important source of afferents for the limbic system, its involvement may be one of the factors underlying both cognitive changes and PET abnormalities.

Electrocorticography in patients with medically intractable temporal lobe seizures. I. Quantification of epileptiform discharges prior to resective surgery

We studied retrospectively the intraoperative preresection electrocorticograms (ECoGs) of 72 patients undergoing surgery for medically intractable, mostly complex partial, temporal lobe seizures (TLS). Quantification of interictal epileptiform discharges (EDs) detected visually at each electrode location in 2 min recording epochs included computations of ED rates (EDs/min) and cumulative voltages (CuVs) (μV/min). Of 6388 EDs, 81% involved the infratemporal surface, 18% the lateral temporal surface and 1% the orbital frontal area. Forty-eight patients (67%) demonstrated multiple (up to 5 or more), temporally independent foci. Dominant foci in medial and lateral infratemporal locations were about equally common and were significantly more frequent than in lateral temporal locations. Rankings of ED CuVs and rates at individual cortical locations defined 4 areas of “relative interictal cortical epileptogenicity.” These were arranged in an orderly pattern with the anterior parahippocampal gyrus and the inferomedial surface of the temporal tip displaying the highest and the lateral temporal and posterior infratemporal cortices showing the lowest propensity to the interictal epileptiform discharge. Individual areas were not characterized by distinct clinical seizure manifestations. Preresection ECoGs provide information on the epileptogenic dysfunction that involves most of the temporal lobe of patients with medically intractable TLS.

Alz‐50 immunoreactive neuropil differentiates hippocampal complex subfields in Alzheimer's disease

The topographic distribution of Alz-50 containing profiles was determined within the hippocampal formation and anterior parahippocampal gyrus by using a monoclonal antibody directed against the A68 protein in normal and Alzheimer's diseased (AD) brains. Although there was a paucity of immunoreactive neuropil in the normal hippocampal complex, there were a few Alz-50 positive neurons that occupied the hippocampal subfield, CA2. In most AD cases, Alz-50 immunoreactive neuropil was prominent in the outer two-thirds of the molecular layer of the dentate gyrus, although a few cases exhibited staining in the inner third of the molecular layer. CA2 was characterized by an increased density of neuropil staining within stratum pyramidale. The neuropil in subfield CA1 was stained densely with Alz-50 in strata oriens, pyramidale, and at the border between strata lacunosum-moleculare and radiatum. Alz-50 immunostained neurites occupied primarily the lateral two-thirds of the subiculum proper, whereas only sparse staining was seen in the adjacent presubiculum. Alz-50 neuropil and neuronal staining displayed three distinct laminar patterns along the mediolateral extent of the entorhinal cortex, whereas the perirhinal cortex exhibited a bilaminar pattern of immunoreactivity involving heavy staining in layers 1-3 as compared to layer 5. In general, the density of Alz-50 neurite staining in the neuropil appeared inversely proportional to the distribution of Alz-50 immunoreactivity within dendritic and somal compartments. Interestingly, the patterns of Alz-50 staining observed in the hippocampal complex in AD coincides with patterns of well-characterized afferent fiber pathways to these regions, thus further supporting the suggestion that hippocampal subfield specific pathology effectively disconnects medial temporal structures from adjacent neocortex in AD.

Reinnervation of the hippocampal perforant pathway zone in Alzheimer's disease.

The perforant pathway originates from the entorhinal cortex of the anterior parahippocampal gyrus and terminates on the outer dendritic branches of the granule cells of the dentate gyrus and pyramidal cells of the subiculum and hippocampus. It carries the principal cortical input to the hippocampal formation. Destruction of the perforant pathway in experimental animals leads to a partial deafferentation of its target neurons, followed by a robust sprouting of acetylcholinesterase (AChE) terminals in the deafferented perforant pathway zone. In Alzheimer's disease, the cells of origin of the perforant pathway are laden with neurofibrillary tangles. AChE staining in the terminal zone of the perforant pathway in Alzheimer's disease shows several distinct patterns that are not found in control brains. These changes are consistent with the results of experimental studies demonstrating reinnervation in laboratory mammals, including nonhuman primates. The results suggest that in Alzheimer's disease sprouting of AChE-containing systems occurs in the hippocampal formation in response to disease-related cellular damage in the entorhinal cortex.