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Kaneko, Megumi et al., Intrathecally Administered Gabapentin Inhibits Formalin-Evoked Nociception and the Expression of Fos-Like Immunoreactivity in the Spinal Cord of the Rat, J. FIELD OF THE INVENTIONThis invention relates to a method for treating severe tinnitus.BACKGROUND OF THE INVENTIONTinnitus is the perception of ringing, hissing, or other sounds in the ears or head when no external sound is present. Dossier Cuisine La vague "Healthy Food" s'est greffee au continent Europeen apres avoir converti les Americains. Pour beaucoup d'entre nous, avec la rentree, la saison des grandes vacances et des lointaines expeditions est terminee. Tinnitus is the medical term for the perception of sound in one or both ears or in the head when no external sound is present. Although there have been tremendous advances through research, the exact physiological cause or causes of tinnitus are not known. Noise exposure – Exposure to loud noises can damage and even destroy hair cells, called cilia, in the inner ear. Certain disorders, such as hypo- or hyperthyroidism, Meniere’s disease, Lyme disease, fibromyalgia, and thoracic outlet syndrome, can have tinnitus as a symptom. Ototoxicity – Some medications are ototoxic, that is, the medications are harmful or damaging to the ear. Although there presently is no cure, in some cases, tinnitus can be managed by treating the underlying cause or by altering reactions to it. The phrase “prevention is the best medicine” could have been coined specifically for tinnitus. When poor physical health is to blame for tinnitus, correct the underlying medical issue(s) are sometimes all it takes to get rid of the ringing in the ears. While it is not clear exactly why they work, certain antidepressant medications can correct or reduce tinnitus. Benzodiazepines (most famously, Valium and Ativan) have been tried in tinnitus with mixed results. When tinnitus is a symptom on Meniere’s disease, surgical therapy might be able to correct the dizziness and ear fullness while at the same time eradicating tinnitus. While they have not yet been perfected, there are various types of electrical and mechanical devices that have been used to treat tinnitus. A tinnitus masking device is quite similar to a hearing aid in form but not necessarily in function. My foundation in faith and family has allowed me to face challenges and grow into an expert in hearing health care. DEAR MAYO CLINIC: For the past several months I have had a high-pitched ringing in my ears.
ANSWER: Tinnitus involves hearing noise in one or both ears that is not caused by an external sound. The noise of tinnitus often sounds like a ringing in the ears, but it can also be buzzing, clicking, roaring or hissing. You need additional evaluation to see if the cause of your tinnitus can be found and treated. If the hair cells inside your inner ear are broken, bent or otherwise damaged, they may spark random electrical impulses to your brain, causing tinnitus. Reviewing your medical history with your primary health care provider, along with getting a thorough physical exam and having diagnostic tests, can help provide vital clues to the cause of your tinnitus. In many cases, a hearing exam completed by an audiologist is a key part of a tinnitus assessment. If an evaluation reveals an underlying condition, then treatment for that condition often relieves tinnitus. The Heart of the Matter: What Does America Really Know about Coronary Artery Disease Treatments? The clinical significance of QEEG LORETA data analysis performed sequentially within 6 months is presented in a case report of a predominantly central type severe disabling subjective idiopathic tinnitus (SIT) before and following treatment.
Keywords: absolute power, asymmetry, coherence, comorbidities, functional brain imaging, QEEG Loreta, relative power, source localization. The QEEG was introduced by Weller and Brill in the 1990s for diagnosis and treatment of tinnitus patients1.
Since 2006 the QEEG has been introduced into the medical audiologic tinnitus patient protocol (MATPP) for the evaluation and treatment of a predominantly central type severe disabling subjective idiopathic tinnitus (SIT). Source localization with LORETA of the maximal abnormality in the very narrow band frequency spectra has identified since 2012 the mathematically most probable underlying sources of the scalp recorded data. In 2014 QEEG data was presented in a SIT patient with a cochlear implant (CI) soft failure before and after treatment attempting tinnitus relief both with conservative pharmacologic medications and following surgical removal of the initial cochlear implant and reimplantation with a new CI. It was suggested that a clinical application of the QEEG be extended to all SIT patients 1) to provide objective data to map brain wave activity reflective of multiple brain function activity in the presence of the tinnitus signal and 2) provide an objective method to identify treatment efficacy in terms of "normal", "abnormal" brain function brain wave activity8.
Both neurometric QEEG evaluations included a twenty minute recording of eyes closed, resting EEG from which two minutes of artifact-free data were selected for quantitative analysis. The patient reported a history of head injury sustained in January 2014, with unremarkable MRI findings upon imaging. A tendency toward low power in all frequency bands, only reaching significance in posterior regions in slow waves (delta and theta frequency bands). A tendency toward excess of relative power (%) in the beta frequency band, only reaching significance in the right central and midline regions. Within both hemispheres between frontal and occipital regions in slow frequencies (Frnt > Occip), between frontal and midline regions and between midline regions in the beta frequency band (central midline having greatest power). Within the right hemisphere between anterior and posterior regions, in slow frequency bands and in all cases with more anterior regions having greater power than more posterior regions.
Hypocoherences between frontal and more posterior regions and between frontal and central midline regions in the beta band and between frontal regions in the theta band.
Maximal abnormality in the narrow band frequencies was found in the beta band in cortical and subcortical sources. Hypercoherences in delta, theta and alpha bands between left dorsolateral prefrontal region and ipsilateral short distances. Visual inspection of the EEG record revealed beta bursting throughout the record at the vertex region. Source localization of the maximal abnormality in the very narrow band frequency spectra (24.1 Hz) showed the mathematically most probable underlying sources of the scalp recorded data to be greatest in the Thalamus, caudate nucleus, anterior and posterior cingulate. A tendency toward low power in all frequency bands, reaching significance in alpha band especially in the central, parietal and occipital regions and in the theta band in the occipital, temporal and fronto-occipital regions. A tendency toward excess of relative power (%) in the beta frequency band, only reaching significance in the right parietal and bilateral occipital regions. Significant disturbances in power relationships between midline central and frontal, temporal and central regions, with more power in the central midline region.
Coherence and cortical connectivity (coherence relationships between regions), was considered to be within normal limits. This patient's neurometric QEEG analysis of the broad band frequencies (delta, theta, alpha, beta and beta 2) was considered to be largely within normal limits for his age.
Significant disturbances in power relationships were found between the central midline regions and frontal regions (F Pz) in the beta bands. Visual inspection of the EEG record revealed occasional small sharp waves (especially on left hemisphere).
Source localization of the maximal abnormality in the very narrow band frequency spectra (24.21 Hz) showed the mathematically most probable underlying sources of the scalp recorded data to be greatest in the mid-cingulate, bilateral precuneus, cingulate and the bilateral caudate nucleus. Comparisons to the neurometric database to evaluate the likelihood that a patient's neurometric profile statistically resembles that seen in patient populations with specific clinical conditions should be made in the drug-free condition and not in the presence of head injury. While both evaluations showed a tendency toward low power in all frequency bands, the prior exam found this to be most noted in delta and theta, while the current evaluation found this to be maximal in the alpha and theta bands, suggesting a shift in the frequency spectrum. Narrow band abnormalities and maximal peak in the LORETA spectra were found in both evaluations to be in the high beta frequency band with most probable underlying sources of the scalp recorded data to be greatest in similar regions with the current evaluation showing more involvement of the precuneus and less involvement of the Thalamus compared with the prior exam. Tinnitus initial onset, described as when patient was awake and "hours" following exposure to the noise of a race car "greater than 100 dB". The initial quality of the tinnitus was the "tea kettle", followed by the "steam "a month later.
An overall weight loss of 30 lbs, diet related, was 15 lbs prior to the tinnitus onset and additional 10-15 lbs.
Visual analog scales of intensity and depression, the Tinnitus handicap inventory, Beck's depression index- all were consistent with SIT. 3) With respect to power relationships between and within hemispheres, both evaluations found this to be maximal in the beta frequency band and involving midline central regions (Figures 1, 2, 3, 4 and 5). 4) The significant disturbances previously reported in coherence and cortical connectivity (coherence relationships between regions), were found to be largely normalized in this evaluation.
6) adjunct function clinically considered to support the central component of the tinnitus diagnosis; and depression. 7) discriminant function analysis for specific comorbidities based on the data and its correlation with the clinical history, eg Head and neck trauma, and depression. The hyper and hypo connectivities in and between the central electrode recording site(s), the caudate nucleus and insula, and the source localization of maximal abnormality in the narrow band frequency spectra (24.21 Hz), mid-cingulate, bilateral precuneus, cingulate and the bilateral caudate nucleus clinically is hypothesized to reflect pathophysiological processes between the cortex and striatum involving the dopamine system. Significantly, in this patient the hyper and hypo connectivities and the source localization data in both studies are non auditory and not auditory ROIs. 3) With respect to power relationships between and within hemispheres, both evaluations found this to be maximal in the beta frequency band and involving midline central regions (Figure 1, 3 and 4).
The significant disturbances previously reported in coherence and cortical connectivity (coherence relationships between regions), were found to be largely normalized in this evaluation with persistence of the ROIs caudate and cingulate. Primary comorbidities were highlighted by "tinnitus" and head trauma, but by components of the aberrant auditory sensation, the SIT, i.e. The significance of the caudate scores in this patient, specifically for a correlation with PTSD, to be determined by the clinical course of the SIT patient. The Z score for the caudate rt > lt ROI may clinically reflect PTSD in this patient in which the initial trauma was the tinnitus. The caudate nucleus is a structure that has been implicated in the neural circuitry of psychological responses to trauma. In general, converging evidence was reviewed from multiple domains including anatomical studies of corticostriatal circuitry, neuroimaging studies of healthy volunteers, patient studies of performance deficits on a variety of cognitive tests, and animal studies of behavioral control. Clear evidence has been demonstrated of an association between a smaller amygdala volume and PTSD.
It is hypothesized that the clinical course of a particular type of SIT, can be viewed from the paradigm of a medical trauma, (i.e. The complexity (ies) of the tinnitus for this patient both for tinnitus diagnosis and treatment was compounded by the presence of comorbidities and reflected in the initial QEEG data.
The sequential QEEG data reflected the results of the initial combined treatment protocol, a tinnitus targeted therapy (REF Palliation 2004), based on a rationale of translation of principles of sensory physiology. The SIT patient in general is fearful of the present and his future, particularly when informed that there is no cure for the tinnitus at this time. Neurologic consultation was recommended for evaluation treatment CNS disease, clinically manifested by complaints of headache, cognitive and sensory disorders. Treatment of the somatosensory complaint included pain management consultation from psychiatry with anesthesiology. Significantly, in this patient the hyper and hypo connectivities and the source localization data are non auditory and not auditory ROIs. Appreciation is expressed to the Martha Entenmann Tinnitus Research Center, Inc for support of this educational effort Leslie S.
The method of the present invention comprises implanting a catheter into a patient and administering a drug formulation or fluid comprising a therapeutic agent intrathecally into the patient's cerebrospinal fluid. The method of claim 1, wherein the solvent comprises an effective amount of NaCl to make the drug formulation isotonic. The method of claim 1, wherein the drug formulation is substantially free of preservatives. The method of claim 1, wherein the at least one therapeutic agent comprises a GABAB agonist.
The method of claim 10, wherein the infusing baclofen comprises a daily dose between 20 and 2000 mcg. The method of claim 10, wherein the infusing baclofen comprises a daily dose between 50 and 1500 mcg. The method of claim 10, wherein the infusing baclofen comprises a daily dose between 100 and 1000 mcg.
The method of claim 1, wherein the at least one therapeutic agent comprises a thyrotropin-releasing hormone. The method of claim 1, wherein the at least one therapeutic agent comprises sodium valproate. The method of claim 1, wherein the at least one therapeutic agent comprises a GABAA agonist.
The method of claim 1, wherein the distal end of the catheter is placed in subarachnoid space between fifth thoracic and first cervical vertebrae. The method of claim 1, wherein the distal end of the catheter is placed in subarachnoid space between fifth lumbar and fifth thoracic vertebrae. The method of claim 26, wherein the gabapentin delivered comprises a daily dose between 1 and 200 mg. The method of claim 26, wherein the gabapentin delivered comprises a daily dose between 1 and 150 mg. The method of claim 26, wherein the gabapentin delivered comprises a daily dose between 2 and 60 mg.
The method of claim 26, wherein the distal end of the catheter is placed in the subarachnoid space between fifth thoracic and first cervical vertebrae. The method of claim 26, wherein the distal end of the catheter is placed in the subarachnoid space between fifth lumbar and fifth thoracic vertebrae. The method of claim 35, wherein the solvent comprises an effective amount of NaCl to make the drug formulation isotonic.
The method of claim 39, wherein the distal end of the catheter is placed in the subarachnoid space between fifth thoracic and first cervical vertebrae.
The method of claim 39, wherein the distal end of the catheter is placed in the subarachnoid space between fifth lumbar and fifth thoracic vertebrae. The method of claim 42, wherein the solvent comprises an effective amount of NaCl to make the drug formulation isotonic.
The method of claim 46, wherein the distal end of the catheter is placed in the subarachnoid space between fifth thoracic and first cervical vertebrae. The method of claim 46, wherein the distal end of the catheter is placed in the subarachnoid space between fifth lumbar and fifth thoracic vertebrae. The method of claim 49, wherein the solvent comprises an effective amount of NaCl to make the drug formulation isotonic. Method for treating tinnitus, the method comprising of: intrathecally administering drug formulation comprising at least one therapeutic agent and a solvent in an amount effective to treat tinnitus. In general, there are attempts to stimulate the ear itself, and attempts to modulate tinnitus through stimulation of muscles in the head or neck (generally termed TENS ).
De la junk-food oui, mais quitte a manger tant de gras sans compter les calories, autant privilegier le gout et la qualite des produits, non ? Alors, ou mange t-on le meilleur burger de Paris ? Rares sont celles qui arrivent a s'en passer, surtout nos blogueuses qui sont ultra connectees ! Les marches de Noel permettent de s'organiser un veritable tour de France a l'occasion des fetes de fin d'annee. There are, however, several likely sources, all of which are known to trigger or worsen tinnitus. When tinnitus is a symptom of another disorder, treating the disorder can help alleviate the tinnitus.
This kind of tinnitus can be caused by abnormal blood flow in arteries or veins close to the inner ear, brain tumors or irregularities in brain structure. However it is important to note that these options do not work for everyone and do not work to the same degree for each individual patient.
Balancing thyroid hormone, correcting anemia, and controlling cholesterol might be all that is required to reverse tinnitus. While some have argued that tinnitus and depression are linked, it is not so simple to think that depression alone leads to tinnitus. These medicines quiet electrical activity in the brain and can be helpful in quieting some of the signals that cause tinnitus. If there is a physical problem that is causing tinnitus and it can be reached and corrected surgically, surgery becomes the treatment of choice. In Meniere’s disease there is an excess of endolymph (fluid) in the vestibular system (the inner ear organ that helps us walk upright and maintain balance). Since once of the root causes (or pathways, really) of tinnitus is abnormal electrical activity in the nerves going from the cochlea to the auditory cortex, scientists and doctors have tried to use electrical stimulation to override those signals. Instead of stimulating the cochlea, a device is applied to the outside of the skull and stimulates brain tissue using strong magnetic oscillations.
These tinnitus treatments include hearing aids, masking devices, and tinnitus feedback retraining.


While a hearing aid amplifies sounds that enter the ear, a tinnitus masking device creates noise of its own.
If after that assessment the cause remains unclear, then you and your health care provider should discuss how to best treat your symptoms. Some of the ear conditions that can lead to tinnitus include exposure to loud sound, age-related hearing loss, earwax buildup and changes within your ear bones. Other conditions that can cause it include cardiovascular disease, allergies, anemia and some jaw disorders. You may be referred to an otologist for a more thorough evaluation of your ears and possible cause of your tinnitus. This test involves listening for sounds played through earphones into one ear at a time and signaling when you can hear the sounds. If the cause cannot be identified, then talk to your health care provider about treatment to help ease tinnitus. A descriptive analysis-interpretation of quantitative electroencephalography (QEEG) data for the metric of power in patients with tinnitus of the severe disabling type (N = 61) was reported in 20063. The electrophysiologic data, correlated with the clinical neurotolgic history and results of the physical examination and clinical course of the SIT, has been provided to the tinnitus professional and SIT patient as an adjunct to increase the diagnostic accuracy for the SIT, attempts to establish its medical significance, translation for selection of treatment modalities attempting tinnitus relief, an objective monitoring function of treatment efficacy, and discriminant function analysis for a identification of a particular diagnostic clinical category of CNS neuropsychiatric disease. The utilization and application of the QEEG data provided objective evidence of altered brain wave activity which correlated with the subjective complaint of the SIT patient, i.e.
Patient also reported depression prior to tinnitus onset of approximately 4-6 months duration. Medications may normalize an abnormal QEEG profile; they may also produce abnormal QEEG features in a normal record, therefore caution should be used in interpretation of this evaluation. Patient also reports history of tinnitus since September 2014 and current depression, cervical disc. The tendency toward excess of relative power (%) in the beta frequency band seen in the prior evaluation was also seen in this evaluation although more posterior.
The tinnitus severity was "immediate", with "anxiety and panic", associated ear blockage bilateral rt > lt, and hypercusis. The increased tinnitus intensity with pressure on the forehead and jaw clenching was noted immediately, i.e.
The node was reported to be singular, not associated with other regional lymphadenopathy, blood test abnormality. Sound attenuation therapy- tinnitus relief, TII 0-2; residual inhibition increased from approximately "a minute" to "several minutes". Electrophysiolgic data - a spectral analysis of the raw EEG data for frequencies of brain wave activities analyzed for the metrics of absolute power, relative power, asymmetry and coherence. Source localization- the maximal abnormality in the very narrow band frequency spectra which shows the mathematically most probable underlying sources of the scalp recorded data. Comparison of frequencies of brain wave activities at two sequential test dates of a 6 month interval of time. Electrophysiologic and source localization data of comorbidities coincident with the chief complaint of the patient. QEEG, for the metrics of absolute power, relative power, asymmetry, coherence - both hyper and hypo coherences and cortical connectivity, when compared to a normative data base, i.e. Clinically this is a demonstration of the monitor function of the QEEG for treatment efficacy (Figures 1, 2, 3, and 4). Clinically this is a demonstration of the monitor function of the QEEG for treatment efficacy. Clinically the physical displacement can be explained and accepted as movement of intracranial contents, solid and fluid, within a closed container, the skull. Simultaneous Initial psychiatric consultation was obtained for the affect behavioral emotional component of the SIT. A study design was aimed to quantify the volume of the caudate in persons exposed to trauma, after adjustment for the covariates (age, sex, intracranial volume, years since trauma, and number of trauma episodes).
A modular conception of the striatum, consistent with hierarchical models of corticostriatal function through which adaptive behavior towards significant goals can be identified i.e.
Amygdala and hippocampal volumes were computed from automated segmentation of high-resolution structural 3-T magnetic resonance imaging in a case-controlled design with structural magnetic resonance imaging and clinical diagnostic assessments12. Post-traumatic stress symptoms (PTSS) exist on a spectrum, and neural changes may occur beyond the diagnostic threshold of PTSD.
As such when correlated with the clinical course of the SIT, its significance for the presentation of SIT in this patient may be viewed from the paradigm of a medical trauma (i.e. Factors influencing the clinical course of the SIT were identified and treated in the ear, fluctuation in of aeration of the middle ears bilateral, secondary endolymphatic hydrops rt, and in brain, presumed intracranial hypertension. In support of this presumption is the reported position influenced alteration in tinnitus intensity and ear blockage i.e. Initial concern was expressed for a return to excellence in sports, social and business activities. With structural MRI identification of volumetric and structural alterations known to be characteristic of known pathology(ies) is visualized.
The QEEGLORETA data analysis has demonstrated an objectivity for SIT, a subjective aberrant auditory sensory symptom. The QEEG LORETA data analysis lends support for the hypothesis of connectivities between neuronal networks underlying the brain functions activated in the presence of the tinnitus signal. The QEEGLORETA data analysis, correlated with the clinical history and clinical course of the SIT, has provided to the tinnitus professional and SIT patient adjunct information to increase the diagnostic accuracy for the tinnitus, its medical significance, and clinical translation for selection of treatment modalities attempting tinnitus relief, an objective monitoring function of treatment efficacy, and discriminant function analysis for identification of a particular diagnostic clinical category of CNS neuropsychiatric disease. The QEEG LORETA data analysis demonstrates electro physiologically, the clinical heterogeneity of the SIT complaint.
Prichep, PhD Adjunct Professor, Department of Psychiatry, NYU School of Medicine and Chief Scientific Officer, BrainScope Company, Inc. Eggermont, “Effects of salicylate on neural activity in cat primary auditory cortex.” Hearing Research, 1996, pp. On le sait, on peut desormais s'envoler le temps d'un week-end et parvenir a s'evader sans trop s'eloigner. Tinnitus can be intermittent or constant-with single or multiple tones-and its perceived volume can range from subtle to shattering.
Your Elkhart Audiologist, Sharon Hirstein, understands that tinnitus can negatively impact your life, family and work. Sure having tinnitus can be depressing, but only certain types of antidepressants work on tinnitus, specifically tricyclic antidepressants.
Sometimes these arteriovenous malformations, as they are called, are present at birth but more often they develop later in life. In fact, the earliest reports of electrical stimulation of the ears for the treatment of tinnitus date back over a hundred years. The technology has been used to improve drug delivery and reduce auditory hallucinations, but may also be effective in treating tinnitus. Since hearing and tinnitus are intimately related, it makes sense that treating deafness also helps treat tinnitus. My doctor said that it is tinnitus and is quite common, but I am concerned and want to know what could have caused it. In some cases, the sound can be so loud that it interferes with your ability to concentrate or to hear actual sound. Although severe tinnitus can interfere with your hearing, the condition does not cause hearing loss. Other factors such as diet, stress and certain medications can play a role in the development of tinnitus, too. Commonly, an audiologist can assist you in using a hearing aid, white noise machine or another similar device to help mask tinnitus and make your symptoms less bothersome. A significant peak was found in the very narrow band frequency spectra at 24.21 Hz, maximal at the vertex (central midline regions). A significant maxima peak was found in the very narrow band frequency spectra at 23.8Hz, maximal at the vertex (central midline region). There were a few inter-regional coherence relationships which were of note as seen in the images below. However, it is noted that this patients profile did not result in a classification as belonging to the population with major affective disorder. With respect to power relationships between and within hemispheres, both evaluations found this to be maximal in the beta frequency band and involving midline central regions.
Neurometrics, identifies and provides a mathematical, and objective standard of deviation from the normal. The multimetric QEEG patterns of analysis of the spectra of frequency(ies) of the brain wave activities, delta, theta, alpha, beta, and beta 2 do not provide to the clinician and the patient a specificity for a particular etiology for the tinnitus but a sensitivity for the functional insult imposed upon multiple structures of the brain by the head trauma in the presence of the preexistent comorbidities. Trial of Neuromonix and masking resulted in a "rebound effect, ie tinnitus intensity increase during and following sound therapy.
The clinical impression that the clinical course of the SIT be viewed from the paradigm of a medical trauma was proposed by a second psychiatrist.
A significant difference was reported in the right caudate nucleus volume between subjects with PTSD compared with those without PTSD. The QEEG data when correlated with the clinical history, physical examination and clinical course, provided adjunct information for an increase in accuracy for the tinnitus diagnosis, and translation of what is known of the pathophysiology of the pattern(s) of brain wave activity(ies) for sensations in general and specifically tinnitus, the perception of an aberrant auditory sensation. When approaching sleep, there was an anxiety reported for an increase in tinnitus intensity. The ear blockage complaint ear rt > ear lt to be clinically identified by targeting Eust tube, inner, and brain to clinically identify the site of lesion of the ear blockage complaint. Epidural cervical block and steroid injection was performed with reported initial pain and increased tinnitus intensity at C3-C4. All brain images are a reflective of multiple brain functions that are activated in multiple ROIs in brain in response to the tinnitus stimulus. In this patient, at the date and time of the test, the non auditory ROIs predominated, which correlated clinically with the affect behavioral component of the SIT. The interneuronal corticostriatal thalamic network provides objective anatomico-physiologic evidence in support of the hypothesis underlying the concept of a Final Common Pathway for all clinical types subtypes of tinnitus which has been projected for all sensations, normal and aberrant21. Quantitative electroencephalography power analysis in subjective idiopathic tinnitus patients: a clinical paradigm shift in the understanding of tinnitus, an electrophysiological correlate. Integration of fMRI and simultaneous EEG: towards a comprehensive understanding of localization and time-course of brain activity in target detection. H2(15)O or 13NH3 PET and electromagnetic tomography (LORETA) during partial status epilepticus.
Caudate volumes in public transportation workers exposed to trauma in the Stockholm train system. Amygdala volume changes in posttraumatic stress disorder in a large case-controlled veterans group.
Post-traumatic stress symptoms correlate with smaller subgenual cingulate, caudate, and insula volumes in unmedicated combat veterans.
According to the American Tinnitus Association, over 50 million Americans experience tinnitus to some degree and of these, approximately 12 million people have tinnitus to a distressing degree.Approximately 2 million Americans have tinnitus to the point where they are so seriously debilitated that they cannot function on a “normal” day-to-day basis and some may commit suicide. Before taking any medication, make sure that your prescribing physician is aware of your tinnitus, and discuss alternative medications that may be available. The best way to prevent tinnitus are to avoid those things that assault the ears namely prolonged exposure to loud noise, short exposures to extremely loud noise, and drugs that can hurt the ears. A full medical checkup is a good place to start because a great number of potential causes will be checked and addressed if needed. If depression was the sole cause, one would expect that better depression medicines like selective serotonin reuptake inhibitors (SSRIs) would also be the better tinnitus medicines. Also, this class of drugs can be habit-forming, which is why they are used with caution and weighed against their usefulness.
An acoustic neuroma is a benign growth around the nerve that carries electrical signals from the inner ear to the brain. While directly stimulating the auditory system has been reported to help 4 out of 5 patients, the tinnitus returns soon after the stimulation has stopped. Early research indicates that transcranial magnetic stimulation may reduce the symptom of tinnitus for up to six months at a time. Improving hearing with a hearing aid does not always correct tinnitus, but it can be quite helpful to a number of patients with both hearing loss and tinnitus (about half).
A lot of other books have a lot of filter information and I have to spend a long time reading before I get to start implementing the tips. Increased intensity tinnitus reported "in quiet" "at night" and accompanied by increased anxiety. The clinical neurotolgicaudiologic history, and physical examination identified multiple comorbidities, both primary and secondary, highlighted not only by "tinnitus" and the head trauma, but components of the SIT. The onset of tinnitus, is perceived as a severe stressor over which the patient has no control) and a lingering Post-Traumatic Stress Disorder.
Volume of the left caudate nucleus was not significantly different between the PTSD and no PTSD groups. It was concluded that the caudate nucleus contributes to behaviour through two processes: 1) the excitation of correct action schemas and 2) the selection of appropriate sub-goals based on an evaluation of action-outcomes.
A significant reduction in nuchal discomfort and reduction in the effect of cervical and facial pressure points was reported following the epidural block at C1-C2. Clinical significance for each neuroimaging technology is established by correlation with the neurotolgic clinical history, physical examination and clinical course of the tinnitus. Lea & Febiger, Philadelphia, PA1991; Martha Entenmann Tinnitus Research Center, 744 Sparrow Dr.
McGeer, “Age Changes in the Human for Some Enzymes Associated with Metabolism of the Catecholamines, GABA and Acetycholine.” Neurobiology of Aging, 1975, pp. The area is certainly murky, scientifically, but antidepressant medications may be a tool to treat tinnitus in certain patients. Newer strategies for treating abnormal blood vessels include burning them or injecting them with sclerosing agents which causes the vessel to shrink and to die. Meniere’s surgery is not 100% effective at treating the primary disease or tinnitus, but it may be an option for some people. It is not practical to use current methods of stimulation constantly—there would be no time for living life. Imaging exams, blood tests and other procedures may be necessary, as well, depending on your medical situation. Fortunately, I was able to get rid of the ringing right away, and am really grateful for this. The LORETA analysis provided a source localization for the scalp surface recorded electrical potential. As such, the patient is sensitized by the initial onset of tinnitus symptoms, experiencing intense anxiety as this new diagnosis represents a constant irritant, a loss of his 'perfect' self, and a regular reminder of that imperfection. The severity of the head trauma, and significance of the antecedent depression, both not visible with structural MRI of brain was established. As such the patient is sensitized by the initial onset of the sensory component of the tinnitus with an accompanying severe anxiety.
The clinical course of the patient will determine the significance of the caudate activity and diagnosis of PTSD in this SIT patient.
The heterogeneity of responses for tinnitus with each neuroimaging technology reflects in 2015 clinical types and subtypes of a predominantly central type of tinnitus. Regular checkups can catch hormonal and metabolic problems in the early stages before they result in tinnitus. If the blood vessel that is causing the problem is an important one (like the jugular vein) destroying it is not a viable option.
Together, the QEEG LORETA analysis provides to the tinnitus professional and patient a mathematical and visual display of the electrical activity in brain for normal and abnormal aberrant brain function.
This is a severe and unrelenting narcissistic injury for the patient who is an attractive, masculine husband, father, and entrepreneur with no prior medical or psychiatric history.
There is a larger right hemisphere volume of the caudate within those exposed to trauma with active PTSD compared with those without PTSD, superimposed upon a baseline caudate asymmetry10.
The putamen, in contrast, appears to subserve cognitive functions more limited to stimulus-response, or habit, learning11.
The sensory component of the tinnitus, the aberrant auditory sensation, predominates in the initial clinical course of the tinnitus complaint.
To clinically remember is the multifunctionality of a single ROI in response to a specific sensory stimulus, and etiology. Similar tissue growths at various places in and around the ear can cause tinnitus and can be cured surgically.
While these devices are primarily used to give the sense of hearing to the deaf, they do so by directly stimulating the cochlea. When the tinnitus intensity index, (TII), a visual analog scale of 0-7 where 0 is no tinnitus perception and 7 = worst intensity - if 5 or above - supplemental.
Images were analyzed using voxel-based morphometry, and regressed against the total CAPS score and trauma load. The intensity of both the sensory and affect components fluctuate in intensity and in the clinical significance to the patient.


While it would be considered a rather bold clinical move, cochlear implants may be used to treat tinnitus in the future.
Group contrast revealed smaller subgenual (sg) anterior cingulate (ACC), caudate, hypothalamus, left insula, left middle temporal gyrus (MTG), and right medial frontal gyrus (MFG) in the PTSD group. Gradually in some SIT patients it may be superseded by and fluctuate in intensity and annoyance with the affective behavioral emotional component, which may become predominant and most significant to the patient.
His level of hypervigilance is more than merely psychological; his sympathetic nervous system is overactive. PTSS are associated with abnormalities in limbic structures that may underlie the pathophysiology of PTSD. Initially the tinnitus intensity increased within 24 hours and was reduced to a TII = 0, hours duration with average of 2 in the following 24 hours of days duration and return to average TII 2-3 in the Am with arising from sleep and average of 3-4 during the day. An overactive sympathetic nervous system has a positive feedback effect on tinnitus intensity. These abnormalities were reported to exist on a continuum with PTSS, beyond a diagnosis of PTSD13. The patient becomes hyper vigilant for any irritant that may increase the intensity of sensory component of the tinnitus, e.g. It is this severely affected population, which is only poorly managed with therapies available today, that may benefit from intrathecal pharmacotherapy proposed in the current investigation.In terms of population percentages, approximately 17% of the general population, and 33% of the elderly population suffer from tinnitus. The quality of life of the patient has been compromised, confusion develops when alone, particularly as reported with interference in sleep, and cognitive function. The level of awareness and hypervigilance of the patient is translated to an overactivity of the sympathetic nervous system9.
There is an activation of the classical "fight or flight" syndrome and resultant upset in the homeostasis of brain function17. Most of the therapies that are presently available attempt to minimize the patients' awareness of the tinnitus symptoms or reduce their emotional reaction to their condition.Rational treatment for the small proportion of patients with a reversible cause for their tinnitus involves correcting the underlying condition. In its simplest form, masking consists of self-exposure to background noise such as, radio, television, or recorded music. People with normal hearing and severe tinnitus can wear a small hearing-aid-like device that produces background (masking) noise in the affected ear. Patients with concomitant impaired hearing and tinnitus sometimes benefit (both their hearing and tinnitus) from use of a conventional hearing aid.PsychotherapyLimbic structures of the brain may be involved in the neural plastic changes associated with tinnitus.
Supportive of this notion is the observation that the perceived amplitude of the tinnitus often does not correspond to the overall severity of the condition. For example, some patients with tinnitus of a relatively low volume are extremely disturbed, whereas others with high volume tinnitus are relatively unaffected by it.
Habituation is a psychological technique that trains patients to ignore or minimize their emotional reaction to tinnitus. Habituation is traditionally defined as the disappearance of reactions to sensory stimuli because of repetitive exposure and the lack of positive or negative reinforcement. The most popular version of this therapy, tinnitus retraining therapy, has been developed and popularized by Dr. Treatments tend to be more successful for mild and moderate forms of tinnitus and for cases of shorter duration.Psychoactive DrugsThe drugs most commonly used to manage tinnitus are antidepressants (especially tricyclics) and anxiolytics (valium, alprazolam, buspirone), although they have limited efficacy. Anxiolytics and antidepressants affect the secondary psychological sequelae of tinnitus, rather than the perception of the noise itself.
The neural plasticity associated with tinnitus may involve the formation of new neural connections between the auditory and limbic systems of the brain. Most agents have been administered orally, although several clinical trials attempting to directly administer agents into the ear have also failed to show efficacy.
Unlike other commonly prescribed oral medications that tend to manage only the emotional symptoms associated with tinnitus, lidocaine actually reduces or eliminates the noise. Lidocaine ameliorates tinnitus in approximately 60-80% of sufferers, a result that has been replicated in numerous well-controlled clinical trials. The efficacy of IV lidocaine is greater than the efficacy produced by auditory nerve transection (approximately 50%), suggestive of a central mechanism of lidocaine action. However, locally administered lidocaine (to the ear or cochlea) has been relatively ineffective.
In addition, locally administered lidocaine to the ear has been associated with significant vestibular side effects such as vertigo and nausea. Tinnitus patients effectively treated with IV lidocaine in the short term, usually experience a return of their symptoms shortly after the medication has been stopped. Intravenous lidocaine (bolus administration) has a short duration of action (10-20 minutes) and is metabolized rapidly by the liver (terminal half life of 1.5 to 2 hours in humans). Lidocaine used in the treatment of cardiac arrhythmias is typically diluted with saline, and administered as a precisely-metered IV infusion. Unfortunately in tinnitus patients with healthy heart rhythms, IV lidocaine can induce potentially life-threatening cardiac arrhythmias.
If administered orally, lidocaine is ineffective due to a major first pass effect.BaclofenTinnitus is associated with abnormal spontaneous neural activity at multiple levels within the central auditory pathways. Gamma-amino-butyric acid (GABA) is the main inhibitory neurotransmitter of the mammalian CNS. An example of a GABAB-receptor agonist is baclofen, which mimics in part the effects of GABA.Several studies have correlated age-related changes in the concentrations of GABA and GABAB-binding sites in the Inferior Colliculus (“IC”), the major auditory midbrain structure. Age-related decreases in the enzyme responsible for GABA synthesis (glutamic acid decarboxylase) have been reported in the IC of both rats and humans. Age changes in the human for some enzymes associated with metabolism of the catecholamines, GABA and acetycholine.
In rats, age-related decreases in the levels of GABA and the number of GABAB-binding sites within the IC have also been reported. These biochemical findings may explain why tinnitus is more prevalent among the elderly.In addition to age-related biochemical changes, the inferior colliculus also shows changes in function (increased spontaneous activity) in response to noise exposure or injury to the peripheral auditory system, results commonly associated with tinnitus in humans. In rats, IV baclofen inhibited noise-induced electrical potentials recorded directly from IC neurons. An additional observation suggestive of the inhibitory role of GABA in the normal auditory system comes from clinical reports of auditory hallucinations that are sometimes experienced with baclofen withdrawal in humans. The authors conducted a randomized, double-blinded study after anecdotal reports described patients who experienced beneficial subjective reduction in tinnitus while taking oral baclofen. Not all of the patients had severe tinnitus, and for some, tinnitus was not their primary complaint. Oral baclofen therapy was associated with significant side effects that included sedation, confusion, dizziness, GI upset, and weakness, the combination of which caused 25% of the enrolled patients to drop out of the trial.These side effects are also associated with oral baclofen used to treat spasticity but are typically not a problem when baclofen is administered intrathecally to treat spasiticity.
By acting at GABAA receptors, benzodiazepines act to inhibit neuronal activity and have proven to be useful in decreasing neuronal hyperactivity associated with epilepsy and anxiety.Benzodiazepines are also commonly used in anesthesiology as tranquilizers. In addition to quelling the hyperactive neurons associated with tinnitus, these agents may offer the added benefit of decreasing anxiety, a common comorbidity associated with severe tinnitus. Two drugs in the benzodiazepine family are midazolam and alprazolam, both of which may be useful in the management of tinnitus.GabapentinGabapentin is a GABA-agonist-like drug. Because it does not bind directly to GABA receptors, it is not a true pharmacologic GABA agonist.
On the other hand, it is known that gabapentin produces inhibitory effects like GABA on selective neuronal populations and thus has been useful in treating several diseases characterized by hyperactivity of central neurons including epilepsy and neuropathic pain. Since the pathophysiology of chronic severe tinnitus appears to be similar to neuropathic pain (plastic neural changes leading to central facilitation of synaptic transmission), many drugs that are effective for neuropathic pain may be effective for tinnitus. Indeed, reports both in animal models and humans suggest that oral gabapentin may be useful in reducing tinnitus. Because gabapentin does not readily penetrate the blood-brain barrier, intrathecal delivery should produce higher more effective concentrations of gabapentin in the CNS.Thyrotropin-releasing hormone (TRH)TRH, a peptide neurotransmitter in the CNS, has been suggested as a useful agent for treating both mood disorders and epilepsy by acting primarily to inhibit the activity of glutamine-containing neurons. Glutamine is the major excitatory neurotransmitter of the CNS and may be associated with increased activity of the central auditory neurons involved in tinnitus. The loss of GABA-containing neurons with aging, results in an increased activity of glutamine-containing neurons that may be controlled by supplying exogenous TRH.Sodium ValproateSodium valproate is another agent that is used to treat central diseases of the nervous system associated with increased neuronal activity.
Clinically it is used to treat both epilepsy and as a mood stabilizer to treat bipolar disorder. 5,676,655 discloses a method for implanting a neural prosthetic drug delivery apparatus into a target zone of a patient's brain for reducing or eliminating the effects of tinnitus.
The apparatus includes a catheter that is inserted into the patient's auditory cortex or thalamus. The catheter microinfuses drugs that suppress or eliminate abnormal neural activity into geometrically separate locations of the patient's cortex or thalamus, thereby reducing or eliminating the effects of tinnitus. The patent, however, deals with drug delivery directly into brain tissue or into specific anatomical structures, i.e.
There are a number of disadvantages to intraparenchymal drug delivery to treat severe tinnitus. For example, intraparenchymal drug delivery is relatively invasive and requires a highly trained neurosurgeon to implant the catheter into the brain tissue or specific anatomical structure.SUMMARY OF THE INVENTIONOne or more of the above-mentioned deficiencies in the art are satisfied by the method of the present invention of intrathecal drug delivery for the treatment of severe tinnitus. One embodiment of the invention involves the use of a drug formulation infused intrathecally to treat tinnitus. For example, a catheter is implanted into a patient, the catheter having a proximal end and a distal end. The distal end of the catheter is adapted to infuse the drug formulation intrathecally into a patient's cerebrospinal fluid.
The drug formulation may comprise a solvent and at least one therapeutic agent such as baclofen, gabapentin, sodium valproate, a benzodiazepine such as midazolam or alprazolam, or a thyrotropin-releasing hormone.In one embodiment of the invention, the proximal end of the catheter is coupled to an implantable pump and the distal end of the catheter is inserted into the subarachnoid space of a patient's spinal column. The implantable pump is operated to deliver a fluid that may comprise a therapeutic agent such as gabapentin, sodium valproate, or a thyrotropin-releasing hormone.
2 is a diagrammatic illustration of the location of a patient's inferior colliculus and the flow of cerebrospinal fluid in the subarachnoid space.FIG.
3 is diagrammatic illustration of a catheter implanted in a patient according to an embodiment of the present invention.FIG.
4 is a diagrammatic illustration of an implanted catheter and pump in accordance with an embodiment of the present invention.FIG.
5 is a diagrammatic illustration of a catheter implanted in a patient's subarachnoid space for the delivery of a therapeutic agent or agents into the cerebrospinal fluid.DETAILED DESCRIPTION OF THE PREFERRED EMBODIMENTSAs illustrated in FIG. 1, the central auditory pathways comprise, the inferior colliculus 1, the auditory cortex 2, the dorsal acoustic stria 102, the cochlear nuclei 104, the geniculate nucleus 106, the nucleus of the lateral lemniscus 108, the superior olivary nuclei 110, and the intermediate acoustic stria 112.
Experimental evidence suggests that the dorsal cochlear nuclei 104, the inferior colliculus 1, and the auditory cortex 2, as shown in FIGS. These major auditory structures are relatively shallow brain structures that lie in close proximity to the subarachnoid space 3 as shown in FIG. 2.The inferior colliculus 1 lies on the dorsal surface of the midbrain 4 and rostral (cephalad) to the fourth ventricle 5 and dorsal to the cerebral aqueduct of Sylvius 8. The superficial surface of the inferior colliculus 1 is bathed in cerebrospinal fluid (CSF) 6 that exits the foramina of Magendie and Luschka to flow around the brainstem and cerebellum.
2 indicate cerebrospinal fluid 6 flow.The subarachnoid space 3 is a compartment within the central nervous system that contains cerebrospinal fluid 6. The cerebrospinal fluid 6 is produced in the ventricular system of the brain and communicates freely with the subarachnoid space 3 via the foramina of Magendie and Luschka.As previously discussed in the background of the invention, available evidence suggests that tinnitus arises within the central auditory structures of the brain, and that those structures represent an important target for therapeutic agents. Given the limited efficacy of other treatments, intrathecal delivery of therapeutics into the cerebrospinal fluid 6 in accordance with the present invention offers the potential to reduce the perception of tinnitus in a large portion of severely affected patients who currently have very limited options.The therapeutic agent or agents may include baclofen, gabapentin, sodium valproate, a benzodiazepine such as midazolam or alprazolam, or a thyrotropin-releasing hormone. Each of the agents may be combined with a solvent to form a drug formulation that may be administered intrathecally to a patient. In addition, the drug formulation may comprise an effective amount of NaCl to make the drug formulation isotonic. The drug formulation may have a pH between 4 and 9 and more preferably a pH between 5 and 7. Also, the drug formulation may be substantially free of preservatives and may contain cyclodextrin acting as an excipient to increase solubility.Intrathecal delivery of therapeutics into the cerebrospinal fluid is less invasive than intraparenchymal (direct tissue) delivery of therapeutics.
In addition, intrathecal delivery of therapeutics may not require the need for a neurosurgeon as the delivery of the therapeutics does not require delivery to a direct brain target. Numerous other physicians may be qualified to insert a catheter into the lumbar subarachnoid space of the spinal column in order to initiate intrathecal therapeutic delivery.Referring to FIG.
The device 30 has a port 34 into which a hypodermic needle can be inserted through the skin to inject a quantity of therapeutic agent. The therapeutic agent is delivered from device 30 through a catheter port 37 into a catheter 38.
Catheter 38 is positioned so that the distal tip 39 of catheter 38 is positioned in the subarachnoid space 3 between the fourth cervical vertebrae (C4) 52 and the seventh cervical vertebrae (C7) 54, as shown in FIG. The distal tip 39 can be placed in a multitude of locations to deliver a therapeutic agent into the cerebrospinal fluid of the patient.
In one embodiment, the distal tip 39 of catheter 38 is inserted in the subarachnoid space 3 between the fourth cervical vertebrae (C4) 52, and the seventh cervical vertebrae (C7) 54, to allow for relatively high therapeutic dose infusion concentrations in the intracranial CSF compartment near the inferior colliculus 1 while minimizing spinal exposure. In other embodiments, the distal tip 39 of the catheter 38 is inserted in the subarachnoid space 3 between the fifth thoracic (T5) 49 (FIG. 4) and the first cervical vertebrae (C1) 56, or in the subarachnoid space 3 between the fifth lumbar (L5) 48 (FIG. 3, delivery of a therapeutic agent into the CSF to treat severe tinnitus can be accomplished by simply injecting the therapeutic agent via port 34 to catheter 38.A higher concentration of baclofen delivered intrathecally into the CSF in accordance with the present invention can provide improved reduction of the perception of tinnitus in a large proportion of severely effected patients. Baclofen is a zwitterionic, hydrophilic molecule that does not readily penetrate the blood-brain barrier. The enhanced efficacy and reduced side effects associated with baclofen delivered intrathecally provides higher concentrations of baclofen in CSF than baclofen delivered orally.
For example, pharmacokinetic data shows that baclofen levels in the cisternal CSF, at the base of the brain, after lumbar intrathecal administration are approximately 20-30 times higher in the CSF than levels after oral administration to treat spasticity.
The higher concentration reduces the amount of time between pump reservoir refills whereas the lower concentrations may allow for a greater amount of volume to be delivered intrathecally. In addition, the daily dosage of baclofen to be administered may depend upon the particular treatment protocol to be administered.
Unlike baclofen, which is a selective GABAB agonist, muscimol is a selective GABAA agonist that inhibits neuronal activity by activating chloride channels leading to neuronal hyperpolarization.In addition, a GABAA agonist family of therapeutics, benzodiazepines, may also be intrathecally delivered into the CSF as a therapeutic agent alone or in combination with other therapeutic agents. The benzodiazepines may be comprised of the therapeutics midazolam or alprazolam.A GABA-agonist-like drug, gabapentin, may also be administered intrathecally in the treatment of tinnitus. In addition, the daily dosage of gabapentin to be administered may depend upon the particular treatment protocol.
4, an implantable medical device known as an implantable therapeutic pump 40 is implanted into a patient.
The location of pump implantation is one in which the implantation interferes as little as practicable with patient activity, such as subcutaneous in the lower abdomen.
The proximal end 35 of a catheter 38 is connected to the implantable therapeutic pump outlet. The catheter 38 is a flexible tube with a lumen typically running the length of the catheter 38.
The distal end 33 of catheter 38 is positioned to infuse a fluid into the target area of CSF of the patient. The pumped fluid may comprise a therapeutic agent such as gabapentin, sodium valproate, or a thyrotropin-releasing hormone.
In addition, the pumped fluid may comprise an effective amount of NaCl to make the drug formulation isotonic.The target area of CSF of the patient may be the subarachnoid space 3 between the fourth cervical vertebrae (C4) 52 and seventh cervical vertebrae (C7) 54, as shown in FIG.
In addition, other target areas of the CSF of the patient may include the subarachnoid space 3 between the fifth thoracic (T5) 49 (FIG. 4) and the first cervical vertebrae (C1) 56, or the subarachnoid space 3 between the fifth lumbar (L5) 48 (FIG. The implantable therapeutic pump 40 is operated to discharge a predetermined dosage of the pumped fluid into the CSF of the patient.The implantable therapeutic pump 40 contains a microprocessor 42 or similar device that can be programmed to control the amount of fluid delivery.
A controlled amount of fluid comprising therapeutics may be delivered over a specified time period. With the use of the implantable therapeutic pump 40, different dosage regimens may be programmed for a particular patient. Additionally, different therapeutic dosages can be programmed for different combinations of fluid comprising therapeutics. Those skilled in the art will recognize that a programmed implantable therapeutic pump 40 allows for starting conservatively with lower doses and adjusting to a more aggressive dosing scheme, if warranted, based on safety and efficacy factors.The embodiments of the invention, and the invention itself, are now described in such full, clear, concise and exact terms to enable a person of ordinary skill in the art to make and use the invention.
To particularly point out and distinctly claim the subject matters regarded as invention, the following claims conclude this specification. To the extent variations from the preferred embodiments fall within the limits of the claims, they are considered to be part of the invention, and claimed.



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