Bitemporal Lesions Research Articles

Hrayr Terzian (1925-1988): a life between experimental neurophysiology and clinical neurology.

This article provides a biographic and scientific profile of prof. Hrayr Terzian (Addis Abeba 1925-Verona 1988). In 1966, Terzian was appointed professor of the clinic of nervous and mental diseases in Cagliari, and in 1970 moved to Verona, where until his death he led the Neurology Clinic serving as the first rector of the local university. As a close friend of the psychiatrist Franco Basaglia (1924-1980), Terzian contributed to the reform of the Italian mental health system. His interests and scientific contributions were extremely broad. He was the first to describe the electroencephalographic changes induced by the antipsychotic chlorpromazine and, together with Henri Gastaut (1915-1995) and his wife Yvette, to describe the rolandic arched ("mu") rhythm. He contributed to elucidate the inhibitory mechanisms of the cerebellum on the antigravity postural tone and provided the first description of Klüver-Bucy syndrome in humans. Always attentive to the social and political aspects of medical practice, prof. Terzian achieved outstanding results both in experimental neurophysiology and in clinical neurology. Besides offering a tribute to Hrayr Terzian, this article provides a brief historical overview of the different clinical pictures caused by bilateral temporal lesions: from the first animal observations by Sanger Brown (1852-1928) and sir Edward Albert Sharpey-Schäfer (1850-1935), later confirmed and expanded upon by Heinrich Klüver (1897-1979) and Paul C. Bucy (1904-1992), to the first cases of bitemporal lesions in humans, including that of the famous patient H.M. (Henry Gustav Molaison, 1926-2008).

Herpes encephalitis during natalizumab treatment in multiple sclerosis

In this case report we describe the first non-fatal herpes simplex virus encephalitis (HSE) case with natalizumab for multiple sclerosis (MS). A 36-year-old woman, previously treated with immunomodulatory and immunosuppressive drugs for MS, developed acute encephalitis after 6 monthly natalizumab perfusions. Brain imaging demonstrated suggestive bi-temporal lesions. Herpes simplex virus type-1 DNA was detected in cerebrospinal fluid. The patient improved gradually after a 21-day course of intravenous acyclovir, but neuropsychiatric changes remained 5 months later. Our non-fatal case of HSE and other reported cases of herpes infections provide evidence of an increased risk with natalizumab and point to the need for clinicians to maintain awareness.

Stereotypies after herpetic encephalitis with bitemporal lesions

Stereotypies after herpetic encephalitis with bitemporal lesions

Klüver Bucy syndrome, unusual consequence of excessively rapid correction of severe hyponatremia

Features of Klüver-Bucy syndrome (KBS) include hypersexuality, hyperorality, placidity, visual agnosia, amnesia, hypermetamorphosis, and emotional and nutritional behavior changes. It is a clinical presentation of bitemporal disorders with limbic system abnormalities. The most common cause of KBS is herpes encephalitis. An otherwise healthy 61-year-old woman presented with mental status changes (MMSE-0) after 6 days of severe vomiting. Extracellular dehydration, hyponatremia (107 mmol/L), low levels of natriuresis, and mild hypokalemia were noted. The initial computed tomography (CT) of the brain was normal. Over 36 hours of hospitalization in a district hospital she developed unusual neuropsychiatric disorders: hypersexuality, hyperorality, absence, visual agnosia, sensory aphasia, amnesia, and depression typical of KBS. She was then transferred to a neurology department. Clear improvement was visible 3 months later: MMSE-22, moderation of hypersexuality and hyperorality, partial correction of amnesia and aphasia, regression of visual agnosia. But the prosopagnosia (face blindness) persisted, and the patient remained unable to differentiate positive and negative facial expressions. Intracranial mass, epilepsy, neuromeningeal infection and head trauma were all ruled out. Antiepileptic and antiherpetic agents were tested without success. There was no evidence of adrenal insufficiency or inappropriate vasopressin secretion. Only severe vomiting, corrected by water intake, could explain the hyponatremia. The first MRI showed bitemporal edema; 3 months later it showed large bitemporal lesions, both internal and external, with atrophy of the hippocampus and limbic system. These MRI findings are characteristic of KBS. To our knowledge, this is the only the second case of KBS with bitemporal myelinolysis reported related to excessively rapid correction of hyponatremia (increase of 30 mmol/L over 36 h), which leads more usually to central pontine myelinolysis.

Transient global amnesia triggered by the intracarotid amobarbital procedure

The emergence of a sudden, global, and fully reversible amnestic state during an intracarotid amobarbital procedure (IAP) performed in a patient with a right temporal tumor is described. Forms of amnesia during the IAP are discussed, and it is argued that because of its appearance, the associated behavioral abnormalities, and EEG findings, this state was a transient global amnesia (TGA). In addition to other origins such as bitemporal lesions, increased barbiturate levels, seizures, and epileptic amnesia, TGA may triggered by stress or angiography during the IAP.

Generators of middle- and long-latency auditory evoked potentials: implications from studies of patients with bitemporal lesions

We recorded middle- and long-latency auditory evoked potentials (AEPs) in 5 patients (ages 39–72 years) with bilateral lesions of the superior temporal plane. Reconstructions of CT sections revealed that primary auditory cortex had been damaged bilaterally in four of the patients, while in the fifth an extensive left hemisphere lesion included primary auditory cortex while a right hemisphere lesion had damaged anterior auditory association areas but spared primary auditory cortex. Normal middle-latency AEPs (MAEPs) were recorded at the vertex electrode in all of the patients. In 3 of the 5 patients, MAEPs also showed normal coronal scalp distributions and were comparable in amplitude following stimulation of either ear. Two patients showed abnormalities. In one case, Na (latency 17 msec)-Pa (latency 30 msec) amplitudes were reduced over both hemispheres following stimulation of the ear contralateral to the more extensive lesion. In another, with both subcortical and cortical involvement, the Pa was abolished over the hemisphere with the more extensive lesion. Long-latency AEPs were normal in 2 patients whose lesions were largely confined to the superior temporal plane. In 2 patients with lesions extending into the inferior parietal lobe, N1s were abolished bilaterally. In the fifth patient, the N1 showed a slight reduction over the hemisphere with the more extensive lesion. Middle- and long-latency AEPs were differentially affected by some lesions. For example, patients with absent N1s could produce normal Pas. A review of these results and those of previous studies of bitemporal patients suggests that abnormalities in middle- and long-latency AEPs do not necessarily reflect damage to primary auditory cortex per se, but rather the degree of damage to adjacent areas. Abnormalities in MAEPs are associated with subcortical lesions, or cortical lesions extensive enough to denervate thalamic projection nuclei. Abnormalities in the long-latency N1 reflect lesion extension into the multi-modal areas of the inferior parietal lobule. This area appears to exert a critical modulatory influence over N1 generators outside of the superior temporal plane.

Bitemporal lesions dissociate auditory evoked potentials and perception

We studied auditory evoked potentials (AEPs) in an 82-year-old female patient who became suddenly deaf following the second of two strokes. The patient showed markedly elevated pure tone thresholds, was unable to discriminate sounds and could not understand speech. Brain-stem auditory evoked potentials (BAEPs) were normal. CT scans revealed bilateral lesions of the superior temporal plane which included auditory cortex. Two experiments were performed. In the first, tones, complex sounds and speech stimuli were presented at intensities above and below the patient's perceptual threshold. P1, N1 and P2 components were elicited by each of the stimuli — whether or not they were perceived. In particular, stimuli presented below threshold evoked large amplitude, short latency responses comparable to those produced in a control subject. In a second experiment, the refractory properties of the N1-P2 were examined using trains of tones. They were also found to be similar to those of normal subjects. Shifts in the pitch of the tones near the end of the train (when refractory effects were maximal) evoked N1-P2s with enhanced amplitudes, although the change in pitch was not perceived by the patient. In both experiments AEP scalp topographies were normal. The results suggest that bitemporal lesions of auditory cortex can dissociate auditory perception and long-latency auditory evoked potentials. A review of evoked potential studies of cortical deafness suggests that the neural circuits responsible for N1-P2 generation lie in close proximity to those necessary for auditory perception.

A Case of Cortical Deafness-Deafness due to Bilateral Temporal Lesion

A 50-year-old, right-handed, male showed cortical deafness and Wernicke's aphasia after 14 hours' duration of atrial paroxysmal tachicardia.Neuroradiological study by 90Tm brain scan revealed hot lesions in the temporal area bilaterally and CT scan showed that a low-density area occupied in the both temporal gyri and insulas. The basal ganglia and thalamus (including medial geniculate bodies) were spared bilaterally.1) Pure tone audiometry revealed a bilateral mild hearing loss but the thresholds were unstable.2) Bekesy audiometry showed a temporary threshold shift bilaterally.3) Speech audiometry revealed lower discrimination rate than 25% bilaterally.4) Discrimination rate of musical instruments was remarkably low. Perception of rhythm and melody was markedly impaired.5) Sound localization for warble tone was well preserved.6) Auditory Brain Stem Response by click sounds was normal.7) Wave forms of the middle latency response were almost normal.However, thresholds of the slow vertex response were abnormally high in both ears. Thus, auditory pathway in the peripheral apparatus and brain stem appeared to be almost intact, but functionally, cortical or subcortical lesions were suspected bilaterally, Sensory aphasia was coincident. Other six cases of cortical deafness or auditory agnosia in the literature were reviewed, and the clinical findings and auditory disorders of these seven cases were remarkably similar to those of the case reported herein. In conclusion, we consinered that “auditory agnosia due to bitemporal lesions” for these cases was the better term “cortical deafness.”