Laser hyperthermia using Nd-YAG laser was studied experimentally and clinically to treat deep-seated brain tumors. Histological changes, temperature profile, and modification of the blood-brain barrier were studied using cat and rat brains. In a clinical study 5 patients with brain tumors were treated with laser hyperthermia using this computed tomography-stereotactic technique. All tumors of these patients disap-peared on computed tomography, and 3 of the 5 patients are still alive without reccur-rence. It was possible to make optimal lesion and to have accurate peripheral temperature control by using the combination of the Komai stereotactic method and the SLT Nd-YAG laser system. Interstitial laser hyperthermia using this method is easy and safe to use, and it is beneficial to treat deep-seated brain tumors.
1. An extracellular study of the cat medial thalamus has revealed four types of somatosensory neurons. These were located primarily in the n. parafascicularis, n. subparafascicularis, and n. centralis lateralis; none were found in the n. centrum medianum. There was no functional segregation of neurons within each nucleus or between nuclei. Each type of neuron had large and often bilateral receptive areas. No somatotopic organization of neurons was found within the medial thalamus. 2. Noxious (N) and noxious-tap (NT) neurons comprising 72% of the sample (78 of 109 total) were considered to be nociceptive. N cells responded exclusively to noxious mechanical stimulation of skin, muscle fascia, tendons, and joints, and to direct stimulation of A-delta- and C-fiber groups in cutaneous, articular, and muscle nerves. NT cells responded to noxious and tap stimulation in a differential manner and to stimulation of the entire spectrum of A- and C-fibers. N and NT cells accurately signaled the duration of noxious mechanical stimulation. Their nociceptive responses were also graded as a function of both noxious stimulus intensity and the number of activated A-delta- and C-fibers. Stimulation of A- and C-fibers evoked, respectively, an inital burst and a late burst of discharges. A brief period of inhibition intervened between the initial and late bursts of NT cells. Prolonged afterdischarge was often observed following noxious natural stimulation or stimulation of A-delta- and C-fibers. The phenomenon of discharge "windup" was observed during iterative stimulation of C-fibers. 3. Tap (T) neurons (10%) responded only to brisk but innocuous taps applied to skin or underlying tissue. These cells were driven only by activation of A-alpha- and A-beta-fibers. The response to such stimulation was seen as an initial burst of discharges followed by an inhibitory period. 4. Inhibited (I) neurons (18%) had resting discharges that were inhibited by noxious stimuli and stimulation of A-beta- and C-fiber groups. 5. The results obtained from monitoring the peripherally evoked responses of nociceptive N and NT neurons before and after selective lesions of the spinal cord strongly suggested that the spinothalamic tracts were the only spinal projections mediating A- and C-fiber input to these cells. Each spinothalamic tract apparently carried information originating from both sides of the body.
Considerable skepticism still exists concerning the concept of neurovascular compression (NVC) syndromes of the eighth cranial nerve (8th N). If such syndromes exist, the sites of compression of the nerve must explain the symptoms encountered. We recorded compound action potentials of the cochlear nerve (CCAPs) during neurovascular decompression (NVD) to examine the topography of the three components of the 8th N. The sites of compression of the 8th N in cases of NVC syndrome confirmed at surgery were superimposed on the topography of the CN and vestibular nerve (VN) in order to determine the relationship between the sites of compression and the symptoms. CCAPs were clearly and consistently recorded on the caudal surface of the 8th N along the midline. In patients with vertigo and tinnitus there was vascular compression of the rostroventral (VN) and caudal surface (CN) of the nerve, respectively. In patients with both vertigo and tinnitus, there was compression of both VN and CN. Our findings clearly demonstrate that the symptoms of NVC of the 8th N depend on the part of the nerve that is compressed by blood vessels, and they support the concept of NVC syndrome of the 8th N.
The tonotopic organization of the cisternal segment of the cochlear nerve has an oblique rotatory structure as a result of the rotatory course of the cochlear nerve in the posterior fossa. Knowledge of this tonotopic organization of the auditory nerve in its cisternal course might benefit surgeons who perform microvascular decompression operations for the vestibulocochlear compression syndrome, especially in the treatment of unilateral severe tinnitus.
Forty-three surgical cases were retrospectively analyzed to establish diagnostic criteria and operative indications for vertigo and tinnitus due to neurovascular compression (NVC) of the eighth cranial nerve (8th N). Many NVC syndromes were mistakenly diagnosed as Ménière's disease or benign paroxysmal positional vertigo. NVC was confirmed in 31 of the 43 patients. Neurovascular decompression (NVD) resulted in complete recovery or marked improvement of subjective symptoms in all 19 cases with vertigo (100%), and in 19 of 29 patients with tinnitus (65.5%). Multiple factor analysis revealed that abnormal caloric responses have high diagnostic value for vertigo due to NVC. Vertigo due to NVC is of short duration (a few sec to a few min.) in the early phase of the disease, which becomes longer and hearing becomes impaired as the history of NVC lengthens. Low pitch pulsatile and high pitch continuous tinnitus are probably due to NVC and are cured by NVD if hearing is still preserved. Tinnitus associated with hemifacial spasm is strongly indicative of NVD. Decompression of the 8th N should be performed in the early phase of disease, since cochlear and vestibular functions are irreversibly impaired if NVC continues for a long period of time.
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