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Found 853 results

  1. Post-traumatic Headaches: Subtypes and Behavioral Treatments Thomas Bennett Chronic, recurrent headache commonly follows head injury, and interestingly, it is seen more often in individuals who have experienced minor head trauma than in those more seriously injured. I will describe subtypes and behavioral treatments of the post-traumatic headache. One must realize, however, that headache is only one of a number of symptoms that commonly follow head injury. While it may be the symptom that results in a patient seeking medical treatment following brain or head injury, it may on the other hand be only the "tip of the iceberg". Many patients complaining only of post-traumatic headache are found, under close neuropsychological evaluation, to be concurrently suffering from verbal and communicative disorders, deficits in information processing and reaction time, memory difficulties, problems with perception, and impaired concept formation and general reasoning ability (Alves, Colohan, O'Leary, Rimel, & Jane, 1986). Post-traumatic headaches should also be considered within the context of post-traumatic symptoms in general which are often collectively called the "post concussion syndrome". At this point it may be helpful to briefly consider the "post concussion syndrome" in general because many of the statements that I could make about post-traumatic headaches apply to other post-traumatic symptoms as well. Post-Traumatic Symptoms The basis of post-traumatic symptoms in individuals who have sustained minor head injury (loss of consciousness of 20 minutes or less and post-traumatic amnesia of 24 hours or less) has been debated for over 2OO years. The common use of the term "post concussion syndrome" to describe the symptoms of these patients has a psychological flavor to it. It was (and still is in less informed circles) typical for physicians and psychologists to ascribe symptoms for which there was no obvious organic basis (no hematoma, no penetration of the dura, no contusion of the brain) to neurotic processes or malingering. The modern view of post-traumatic symptoms is that they do indeed have a biological or organic basis. It is now accepted that even mild concussion usually entails some structural damage to the brain (Jennett & Teasdale, 1981). This is not to say that emotional factors do not play an important role in post-traumatic symptoms because it is generally believed that emotional factors can both exacerbate and prolong post-traumatic symptoms that are the result of biological factors. This conclusion underscores the need to employ both biological and psychological interventions in treating patients with post-traumatic symptoms. With respect to malingering, let me point out that its incidence has been vastly overestimated. Symptoms are deliberately exaggerated in a smaller proportion of patients than was previously thought to be the case (Boll, 1982; Rimel, Giordani, Barth, Boll, & Jane, 1981). Neither insurance claims nor pending litigation is a significant factor influencing return to work or social recovery (Irving, 1972; Oddy, Humphrey & Uttley, 1978). A number of symptoms have been identified to follow minor head injury. However, it is not accurate to describe these symptoms as a syndrome as was common practice when using the term "post concussion syndrome". While a given patient may exhibit one, two, three, or less commonly, more of these symptoms, it is rare to see a patient experience all of them (Alves et al., 1986). Post-traumatic symptoms commonly reported after minor head injury include headaches; dizziness; impaired concentration; memory problems; sensory problems including diminished hearing, olfaction, and taste; diplopia; tinnitus; hypersensitivity to noise; insomnia; fatigue; irritability; anxiety and depression. The mechanisms maintaining these symptoms are not always obvious, but some meaningful statements can be made. The problems with dizziness and auditory difficulties are undoubtedly related to concussion of the balance and central auditory processing functions of the inner ear. Decreased olfactory sensitivity is related to strain injury of the axons of the olfactory tract as they enter the brain. I suspect that reports of decreased taste sensitivity do not reflect a decrement in that specific modality, but rather they reflect a loss of gustatory sensitivity secondary to diminished olfactory sensitivity. Hypersensitivity to noise and hyperirritability probably at least partially reflect general diminished inhibitory or gating (filtering out) processes in the brain. Insomnia is a common sequel after head injury; in general, initiation, maintenance, and cycling mechanisms do not operate as efficiently as they should after head injury, presumably because of neural disruption resulting from rotational forces exerted on the brain stem at the time of injury. Loss of concentration and memory problems may be reflective of diminished information processing ability in general. Gronwall and Wrightson (1974) tested information processing ability using the Paced Auditory Serial Addition Test (PASAT). They found that head injured patients who performed abnormally on this test at 35 days post-injury still complained of post-traumatic symptoms; the disappearance of these symptoms correlated nicely with restoration of normal performance on the PASAT. Irritability, anxiety, and depression can all be contributed to by organic factors, but typically, they are more dependent on psychological processes. Coping with head injury produces feelings of loss of self-control and feelings of helplessness and hopelessness. Finding that you can no longer perform efficiently at home, school, or on the job is very stressful, and it can aggravate other post-traumatic symptoms as well. The nature of and basis for post-traumatic headache is more difficult to explain. There appear to be many possible causes for persisting headache after head injury. Some of these include musculoskeletal trauma to the neck, head, and jaw regions, pain in scalp, scars, neuralgia of occipital or supraorbital nerves, precipitation of migraine in predisposed individuals, and occasional serious intracranial complications. Post-traumatic headaches are a significant health problem when one realizes that close to half of all patients discharged from the hospital after minor head injury report persistent headache (e.g., Alves et al., 1986). Subtypes of Post-Traumatic Headaches The vast majority of patients who experience persistent post-traumatic headaches have no intracranial abnormalities to explain their headache pain (Dalessio, 1980). Electroencephalographic (EEG) abnormalities are not correlated with occurrence of post-traumatic headache, but the presence of scalp lacerations is positively correlated (Scherokman & Massey, 1983). At least four or five types of post-traumatic headaches have been categorized including, 1) steady pressure with cap-like distribution, 2) circumscribed superficial tenderness around the impact site, 3) episodic aching or throbbing pain which is typically unilateral, and 4) episodic, unilateral frontotemporal pain with ipsilateral mydriasis and hyperhidrosis. Recently, I have seen more and more cases where patients report unilateral or bilateral pain in the temple region or just superior to it and I will comment on this as a fifth type of post-traumatic head pain. Type 1: Steady Pressure with Cap-like Distribution Type 1 headaches are the most common and persistent variety of headaches that occur after head injury. Patients will often have this type of headache concurrently with one or more of the other types. As indicated, these headaches are described as a steady pressure, often with a cap-like distribution, but more commonly in a circumscribed area elsewhere than the site of the injury. There is usually a deep tenderness present in the neck or shoulder region, and headache can often be reproduced by manual pressure on these tender areas. The intensity of the associated pain is described as being from "mild to very severe". The attacks of pain can recur for many years. Occurring intermittently, the attacks can vary from several hours to as long as ten days duration (Dalessio, 1980). Type 1 headaches are usually made worse by effort stress, coughing, stooping or turning the head. As a result the patient may be functionally incapacitated for engaging in physical activity related to work or recreation. During periods of severe headache of this sort, patients may experience spinning sensations, dizziness, and photophobia (Dalessio, 1980). Finally, these headaches are associated with persistent and sustained muscle contraction in the head, neck, upper back, and shoulders. This can be easily demonstrated through electromyographic (EMG) studies that show excessive levels of muscle contraction in these patients. Medically, these headaches are treated with muscle relaxants, analgesics, amiltryptaline, heat, and massage. They often prove to be resistant to treatments. Type 2: Circumscribed Tenderness Around Impact Site Most patients with Type 2 headaches suffer from Type 1 headaches as well. Type 2 patients have a circumscribed, relatively superficial tenderness of the scalp at the site of the original injury which is often, but not always, associated with a visible or palpable scar (Scherokman & Massey, 1983). In most patients who experience this type of pain, there is spontaneous aching pain at the original site of impact; in some cases, headache pain only occurs when some pressure, such as a hat or a brush, is applied to the site (Dalessio, 1980). Typically, this type of post-traumatic headache pain is described as being "moderate", and usually it resolves within a year after the original injury. It appears to be related to contusion and injury to the scalp vasculature. Type 3: Episodic Aching or Throbbing Pain, Usually Unilateral Type 3 post-traumatic headaches are described as aching, often throbbing pain, usually unilateral in onset. They occur in attacks and are most commonly reported to occur in the temporal regions. They are also sometimes frontal, occipital, or postauricular. The attacks may be of short duration, and they may represent an intensification of symptoms for patients who also experience a background of Type 1 headache. Reported pain associated with Type 3 headaches varies from "mild to severe". The intensity of the pain is increased by effort, coughing, bending, or lying down. Post-traumatic headaches of the Type 3 variety, while usually unilateral in onset often become generalized. They often begin in the morning or are present upon awakening, and they may continue all day. Nausea, vomiting, and anorexia may accompany them. Dalessio (1980) reports that these headaches are not relieved by massage or head but ice bags, cold compresses, and codeine will provide relief. Ergotamine tartrate eliminated this type of pain but did not diminish Type 1 components resulting from excessive muscle contraction. Type 3 headaches are vascular in nature, and they are more commonly seen in patients with a migraine history, even if migraines have been rare or infrequent in the past. This type of headache disorder is related to recurrent painful distention of cranial arteries. For many patients, it represents the precipitation of a serious vascular headache (migraine) disorder in a person already at risk. Type 4: Episodic, Unilateral Frontotemporal Pain With Ipsilateral Mydriasis and Hyperhidrosis Vijayan (1977) has described a type of headache syndrome associated with anterior neck injuries secondary to cervical whiplash (also see Khurana & Nirankari, 1986). In these patients, unilateral, frontotemporal vasodilating headaches are experienced episodically. What makes them unique is that they are accompanied by ipsilateral mydriasis (excessive dilation of the pupil) and facial hyperhidrosis (excessive sweating). When the pain subsides, the patient is left with ipsilateral ptosis (drooping of the upper eyelid) and miosis (excessive constriction of the pupil). In Vijayan's series, patients experienced between two and 12 of these headaches per month. Type 4 headaches are related to damage to the third-order sympathetic neuron in the neck; they reflect localized sympathetic nervous system dysfunction. Patients with these headaches were helped when treated with the beta adrenergic blocking agent, propranolol, in doses of 20-60 mg per day (Vijayan, 1977); they did not respond to ergotamine. Type 5: Pain in Temple or Superior Temple Region A fifth type of headache syndrome, which also typically is accompanied by Type 1 headaches, is an intermittent recurrent relatively steady pain in the region of the temples or just above. The pain may be unilateral or bilateral, and when it is bilateral, it may be described as a band extending from temple to temple. It is also typically accompanied by jaw popping during chewing, leaving no doubt that it is related to temporomandibular joint (TMJ) dysfunction or injury. Many people in our society clench their teeth at night (bruxism) in response to stress. An automobile accident that results in a person striking the windshield or dashboard can easily exacerbate ongoing temporomandibular joint degeneration or significantly displace or injure a healthy joint. High resolution computerized tomography has been shown to be vastly superior to conventional radiography in detecting TMJ degeneration in post-traumatic headache patients (Tilds, Miller, & Guidice, 1986). The increasing availability of magnetic resonance imaging will enhance the detection of these difficulties further. Treatment of TMJ syndrome, whether post-traumatic or not, may require a multidisciplinary approach including orthodontic and surgical treatments, splint therapy, physical therapy, and biofeedback. In summary, at least five distinct headache syndromes can be described in post-traumatic headache victims. With the exception of Type 4, which reflects sympathetic nerve damage, these headaches reflect musculoskeletal and vascular dysfunction that is essentially the same as that seen in chronic headache patients who have not experienced trauma. As with typical chronic headache patients, the head pain experienced by head trauma victims comes in many combinations. As indicated, patients with Types 2, 3, and 5 headaches will often complain of Type 1 headaches as well, and some patients will exhibit symptoms consistent with several subtypes concurrently. A multimodality approach using behavioral treatment interventions will be described next. The use of behavioral treatments for patients with post-traumatic headaches has been discussed in case studies by several investigators (e.g., Daly & Wulff, 1987; Duckro, Tait, Margolis, & Silvermintz, 1985; Muse, 1986). In Behavioral Treatments of Post-Traumatic Headaches, Packard (1979) asked directly, "What does the headache patient want?" and then outlined the stated needs of patients along with physician estimates of those needs. Generally speaking, physicians ranked medication higher than did the patients. The patients gave their highest rankings to the need for information about the causes of their headaches and to the need for relief from pain. The patients' responses thus indicated that education must be an integral part of any headache treatment program. Behavioral treatment of post-traumatic headaches must thus use a multifaceted approach and should include education about headaches and medications for them, physiologic therapies such as physical therapy, therapeutic massage and biofeedback, and cognitive-behavioral therapies aimed at helping the patient acquire pain management skills. Education Let us forever bury the idea that post-traumatic headaches, or headaches in general, are simply psychiatric problems. Clearly, stress can produce or exacerbate headache syndromes, but headaches are best understood by considering both psychological and physiological factors. Their interaction can be understood by an explanation to the patient with post-traumatic headaches. The Vicious Cycle A major failure of the traditional organic-psychological dichotomy is to downplay the interaction among emotional factors, the autonomic nervous system, and elevated levels of muscle tension on head pain levels. Muscle tension levels are commonly elevated in the head, neck, shoulders, and upper back regions after trauma, and this is often not evaluated in diagnostic studies. The muscle contraction can cause additional pain. Similarly, it is clearly the case that emotional arousal is frequently present in these patients. Emotional arousal increases discharge in the sympathetic nervous system. Prolonged excessive discharge in the sympathetic system will in turn exacerbate pain levels by increasing perception of the intensity of stimuli related to pain. Unfortunately, these physical and emotional factors can create a "vicious cycle" in which pain becomes a stressor, eliciting emotional (anger, frustration) and physical (increased muscle tension) factors which then produce more pain (Zimmerman, 1981). The longer this sort of cycle persists, the more difficult it is to break. Diagramming the cycle, explaining it to the patient and then giving homework exercises to disrupt it have been very effective in helping the post-traumatic headache patient break this cycle. This type of exercise is most beneficial if the patient learns techniques to intervene at multiple points in the cycle. When patients have learned about the physiological factors contributing to their headaches and how emotional factors can interact with physical factors to set up a "vicious cycle", they are ready to accept the fact that their pain has both biological and psychological aspects. They can then be assured that their presence in the psychologist's office is not because their physician believes their headaches are "just in their minds". Treatments Medication I find that few patients understand the role of medication in their treatment. It is clear that medications (i.e., analgesics, those which reduce muscle spasms and overall level of muscle contraction, those that reduce emotional arousal, and antidepressants) can be useful in selected patients. The psychiatric medications may or may not produce pain relief because of their psychiatric effects. Benzodiazepines may help because of their muscle relaxant properties; antidepressants may help because they promote serotonin activity in the brain which in turn decreases pain sensations. Patients need to be informed of why they are taking certain medications. One must be careful in using antidepressants, particularly amitryptaline, in treating individuals with post-traumatic headaches. The anticholinergic side effects of these drugs can exacerbate post-traumatic symptoms related to head injury including dizziness, diminished concentration, and memory problems. Patients also typically have a misconception about how effective their medications should be. They often believe that analgesics should eliminate the pain completely. I find that this is an example of a "fix me doc syndrome" that impedes the progress of many patients. Instead of holding the belief that "improvement is outside of their own control" (Barnat, 1986), post-traumatic headache patients need to learn that a certain amount of discomfort will often persist; it is something that must be lived with. If a medication provides no relief, then it is a failure, but medications that provide only partial relief have not necessarily failed. Biofeedback Physiological therapies, including physical therapy, therapeutic massage, and biofeedback, can be effective treatments for post-traumatic headaches. I will only discuss the use of biofeedback therapy in this paper, but let me emphasize that we regularly refer post-traumatic headache patients to certified massage therapists and/or physical therapists as part of their treatment program. These procedures are all complimentary to one another. Biofeedback is a procedure by which a biological signal (for example, skin temperature, muscle tension, heart rate, brain waves) is converted to an easily detected signal, such as a light or a tone, and "fed back" to a patient so that she or he can exert conscious control over that function. Thus, a person might learn to detect and subsequently lower excessive levels of muscle tension in his or her forehead, neck, shoulders, and jaw, or a person might learn to increase the recorded temperature of her or his finger tips. (Cold hands signal excessive sympathetic nervous system discharge and resulting vasoconstriction; they are a sign of stress and a common characteristic of migraineurs.) Biofeedback is not a cure-all, and this treatment is most effective when incorporated into a comprehensive treatment program. Nevertheless, biofeedback treatment has been used successfully for two decades to treat a variety of psychophysiological disorders including muscle contraction and vascular headaches, hypertension, gastrointestinal disorders, pain syndromes, anxiety syndromes, abnormal heartbeats, sleep disorders, and many neurological syndromes including movement disorders and epilepsy. It is also employed in neuromuscular rehabilitation following peripheral or central nervous system damage (Bennett, 1987). I have found it to be of significant benefit for the post-traumatic headache patient, particularly when combined with stress management training. As I indicated in an earlier article (Bennett, 1988), biofeedback training can have both obvious and subtle benefits for these patients. One obvious benefit would be to teach the patient with excessive levels of muscle tension to relax chronically tensed muscles and to be more sensitive to muscle tension levels. This is accomplished through electromyographic (EMG or muscle tension) training. Temperature training in biofeedback can be used to increase vasodilation (decrease sympathetic activity) and thereby decrease the likelihood of vascular headaches. We typically use a combination of these procedures, as both contribute to stress management and relaxation training. All post-traumatic headache patients can benefit from such training. EMG biofeedback is particularly applicable to patients experiencing Type 1 and Type 5 headaches, and temperature training is especially relevant for patients with Type 3 headaches. A more subtle benefit of biofeedback is to teach the patient that he or she can have some control over an aspect of their life (for example, "I can relax my muscles and decrease the severity of my headaches"). The head injured person often has a recent history of failure and frustration, and feelings of "loss of control" or "helplessness" may predominate. By learning to have more control over something as basic as level of muscle tension or skin temperature, the patient can learn that "what I do can really makes a difference". This helps the person to overcome the "fix me doc" syndrome and places him or her in more control of their future in general. Thus, the feelings of failure, loss of control, and helplessness can be attenuated. Cognitive-Behavioral Therapies The usefulness of cognitive-behavioral therapies in pain management and headache treatment programs is well established. A particularly effective use of these principles in the treatment of chronic headache patients has been described by Bakal (1982), whose general program is quite helpful for patients with post-traumatic headaches. I recommend it highly. Two important features of this program are attention diversion and thought management. These methods assist the patient in decreasing the intensity of the pain and in minimizing negative thoughts and dysphoric affect that increase headache severity. In introducing the use of attention diversion and thought management, it is important to explain to the patient that headache pain consists of both sensory and reactive components. The sensory component consists of sensations of pain that are largely determined by changes in the muscles and veins of the head. The reactive (or cognitive) component consists of the thoughts and feelings that accompany headache episodes. There are, in turn, two important aspects of the reactive component. The first is the amount of attention that is directed toward the headache. The second is our interpretation of thoughts regarding, and feelings about, the pain experience. Negative or catastrophic cognitions exacerbate pain by increasing activation of the sympathetic nervous system. The patient being taught attention diversion learns that we normally only focus on one thing at a time, and we are free to attend to whatever we want. Thus, we can influence what we are attending to by shifting our attention from one aspect of our environment to another (internal or external). Finally, it is difficult if not impossible, to stop focusing on one's pain unless one shifts attention to something else. With this general framework in mind, the patient is provided with a number of attention diversion strategies to learn. They are initially practiced during headache-free periods and later applied to times of significant headache discomfort. Turk (1978) provides a variety of attention-diversion techniques, including imagery production, strategies that are relatively easy to master and quite effective in interrupting and/or decreasing the intensity of a headache attack. Thought management deals with helping the patient control negative and/or catastrophic headache-related thoughts and feelings. By now, the patient is quite aware of the role that distressing thoughts play in their headache disorder. He or she is encouraged to understand that distressing cognitions not only increase the pain experienced, but also they interfere with the ability to cope effectively with the headache pain. These thought patterns can be identified and modified. The patient learns that the process of "negative talking", can be reversed, and training is given in how to accomplish this. First the patient is told to be alert to those times when he or she is experiencing distressing feelings and thoughts. Second, the patient learns to use these distressing thoughts as a signal to start making positive self-statements. Third, the patient learns to actively substitute the distressing cognitions with positive, coping-oriented statements (Bakal, 1982). In order to demonstrate this process, the patient is provided with a list of positive statements (Turk, 1979) to be used during different stages of the headache episode. He or she is encouraged to develop his or her own statements as well. Again, this intervention is over-practiced during times when headaches are not present before being put into practice. Conclusions Post-traumatic headache is the most frequent complaint made by victims of minor head injury and is thus of major importance in head trauma rehabilitation. Post-traumatic headaches can be severe and persistent. As a result they can produce a major disruption in the patient's life. Their economic impact is significant in that they can prevent return to work in individuals who are otherwise recovered. Post-traumatic headaches reflect an interaction among organic and emotional factors. For this reason, they are best treated via a multimodality approach that considers all of these factors. For many individuals, participation in such a program results in a complete remission of their symptoms. For others, the end of the program represents an improvement in their symptoms and the beginning of a long-term process of self-managing their headache pain. Most patients arrive at the point where their headaches no longer interfere with their lives. This represents a significant improvement over their prior incapacitation dependency on a variety of medications. In head injury recovery, this is one sign that the victim can once more be in control of her or his future. REFERENCES Alves, E.M., Colohan, A.R.T., O'Leary, T.J., Rimel, R.W. & Jane, J.A. (1986). Understanding post-traumatic symptoms after minor head injury. Journal of Head Injury Rehabilitation, 1, 1-12. Bakal, D.A. (1982). The psychobiology of chronic headache. New York: Springer Publishing Company. Barnat, M.R. (1986). Post-traumatic headache patients II: Special problems, perceptions, and service needs. Headache, 26, 332-338. Bennett, T.L. (1988). Neuropsychological rehabilitation in the private practice setting. Cognitive Rehabilitation, 6(l), 1215. Bennett, T.L. (1987). Neuropsychological aspects of complex partial seizures: Diagnostic and treatment issues. The International Journal of Clinical Neuropsychology, 9, 37-45. Boll. T.J. (1982). Behavioral sequelae of head injury. In P.R. Cooper (Ed.) Head Injury. Baltimore: Williams and Wilkins. Dalessio, D.J. (1980). Post-traumatic headache. In D.J. Dalessio (Ed.) Wolff’s headache and other head pain, 4th ed. New York: Oxford. Daly, E. & Wulff, J. (1987). Treatment of post-traumatic headache. British Journal of Medical Psychology, 60, 85-88. University Press, 3324-3381. Duckro, P.N., Tait, R., Margolis, R.B. & Silvermintz, S. (1985). Behavioral treatment of headache following occupational trauma. Headache, 25, 328-331. Gronwall, D. & Wrightson, P. (1974). Delayed recovery of intellectual function after minor head injury. Lancet, 2, 605-609. Irving, J.G. (1972). Impact of insurance coverage on convalescence and rehabilitation of head injured patients. Connecticut Medicine, 36, 385-391. Jennett, B. & Teasdale, G. (1981). Management of head injuries. Philadelphia, D.A. Davis. Khurana, R.K. & Nirankari, V.S. (1986). Bilateral sympathetic dysfunction in post-traumatic headaches. Headache, 26, 117-121. Muse, M. (1986). Stress-related, post-traumatic chronic pain syndrome: Behavioral treatment approach. Pain, 25, 389-394. Oddy, M., Humphrey, M. & Uttley, D. (1978). Subjective impairment and social recovery after closed head injury. Journal of Neurology, Neurosurgery, and Psychiatry, 41, 611-616. Packard, R. (1979). What does the headache patient want? Headache, 19, 370-374. Rimel, R.W., Giordani, B., Barth, J.T., Boll, T.J. & Jane, J.A. (1981). Disability caused by minor head injury. Neurosurgery, 9. Scherokman, B. & Massey, W. (1983). Post-traumatic headache. Neurologic Clinics, (2), 457-463. Tilds, B.N., Miller, P.R. & Guidice, M.A. (1986). The diagnostic value of high resolution computerized tomography in post traumatic head pain patients. Headache, 26, 117-121. Turk, D.C. (1978). Cognitive behavioral techniques in the management of pain. In J.P. Foreyt & D.P. Rathjen (Eds.) Cognitive behavior therapy: Research and application. New York: Plenum Publishing Company. Vijayan, N. (1977). A new post-traumatic headache syndrome: Clinical and therapeutic observations. Headache, 17,19-22. Zimmerman, M. (1981). Physiological mechanisms of pain and pain therapy. Triangle, 20, 7-17. This article originally appeared in The Journal of Cognitive Rehabilitation, Volume 6 Issue 2, March/April 1988.
  2. I checked e-benefits today and I went from the Gathering Dust phase to PREPARATION FOR DECISION. I was some comfortable complaining about the Gathering Dust phase that the movement to PREP is feeling almost scary. Interesting that the VA just figured out that they forgot to include hypertension in my C&P last year and sent me a letter last week to report for another C&P this week to take my BP. Driving 2.5 hours to take a BP measurement is really absurd when I have a clinic 10 minutes from my house. On Wednesday I checked e-benefits to see if anything had changed. At that point still gathering military dust. Just needed to spout off and perhaps some emotional support. Been at this claim for about 20 months now. It was finally farmed out from Cleveland to Fargo and has moved rather quickly since Fargo has been on it. They called to ask some questions about the unemployability. Figured out what was missing and holding up the claim.
  3. Yesterday, I received the Judgment from the Administrative Law Judge that handled my appeal. I am using a VA-trained/approved attorney and the judge found in our favor. After 40 years of fighting with the VA. I filed my original claim the second day after my discharge. It was denied over and over again for all these years. I think what made a difference this time was the attorney pointing out that my VA psychologist that I'd been seeing for years, had diagnosed me and then the VA sent me to a specific non-VA psychologist for my C&P and she diagnosed me the exact same way and advised that I should receive a 100% rating for my PTSD. They denied the claim (again) and when I got the decision letter explaining all the evidence they used to make their decision, they didn't include the report from my shrink or the C&P shrink. So, now that service-connection is founded and they've already determined my rating (from the C&P already done), do I too have to go back to sleep for months and months? Sadly, my attorney is on vacation (of all the times to go on vacation...) and his paralegal doesn't feel comfortable telling me what to expect next...
  4. I just received notification from the BVA that I am entitled to SC for hypertension, to include as secondary to SC for OSA and PTSD from an appeal of a denied clam for hypertension in 2004, and from a denial for SC for hypertension secondary to PTSD and or OSA in 2008. The letter from the BAV stated that my records are being sent back to the VA office that has jurisdiction over this matter. What happens next? The letter from the BVA did not state what percentage of disability for hypertension have been awarded, will the RO?
  5. Can anyone tell me if Obstructive Sleep Apnea and Hypertension be secondary to CAD. Also the C&P examiner copied and pasted into my Heart Condition DBQ the following statements from my last cardiology exam. . CC: 1st visit today. Pt w/ h/o chronic, stable angina - reported CP in service in 9/1990 - had NL MPI. Has undergone heart CATHs (1993, 2008), which were NL except as noted below - advised he likely his microvascular disease, or microspasm, or (cardiac) syndrome X (decreased blood flow in LAD). Info in scanned records. Pt has noted intermittent CP >25 years - avg 3x per month - occurs at rest or during sleep or w/ activity - pausing/resting typically relieves - uses one SL Nitro tab on avg of 1x per month to relieve CP. The C&P examiner used the above cardiology exam as a Interview-based METs test because the limitation in METs level is due to multiple medical conditions including the heart condition, it is not possible to accurately estimate the percent of METs limitation attributable to each medical condition. Based on the above statements from the Cardiologist could my SC heart condition be increased from 10% to 100%. i. was also hospitalized in Dec 2016 for my heart condition in which a ECHO and Nuclear Stress Test was performed. My stress test showed I have a EF of 60%. But my ECHO revealed that I have the following: Left Ventricular Basal Septal Hypertrophy, Left Ventricular Diastolic function abnormality with Mild (grade 1) showing impaired relaxation and Trace Mitral and Valve Regurgitation. I also have a history of a past Myocardial Infarction when I was on active duty.
  6. I took the liberty to put up the VA ratings for HTN (Hypertension aka High Blood Pressure). This might help some people with questions. I think if you take all your readings from the past and present and put into a spreadsheet with dates and places then take an average of all the readings. If it falls into these categories, then that can help substantiate your claim, but this is just my opinion, so don't go crazy if your case is different. 7101 Hypertensive vascular disease (hypertension and isolated systolic hypertension): Diastolic pressure predominantly 130 or more............................................................. 60 Diastolic pressure predominantly 120 or more............................................................. 40 Diastolic pressure predominantly 110 or more, or; systolic pressure predominantly 200 or more............................................................................ ....... 20 Diastolic pressure predominantly 100 or more, or; systolic pressure predominantly 160 or more, or; minimum evaluation for an individual with a history of diastolic pressure predominantly 100 or more who requires continuous medication for control......................................... 10 Note 1: Hypertension or isolated systolic hypertension must be confirmed by readings taken two or more times on at least three different days. For purposes of this section, the term hypertension means that the diastolic blood pressure is predominantly 90mm. or greater, and isolated systolic hypertension means that the systolic blood pressure is predominantly 160mm. or greater with a diastolic blood pressure of less than 90mm. Note 2: Evaluate hypertension due to aortic insufficiency or hyperthyroidism, which is usually the isolated systolic type, as part of the condition causing it rather than by a separate evaluation. Note 3: Evaluate hypertension separately from hypertensive heart disease and other types of heart disease.
  7. Here's a listing of my disabilities from the "blue" ratings sheet: 9411 PTSD 100% 9411 PTSD w/alcoholism 100% 7913 Type II Diabetes 20% 6260 Tinnitus 10% 7101 Hypertension associated w/PTSD w/alcoholism 10% 8520 L leg PN associated w/diabetes 10% 8520 R leg PN associated w/diabetes 10% bilateral factor of 1.9% for diagnostic codes 8520. Any thoughts on SMC?? pr
  8. Good Morning. I hope the collective minds at HadIt.Com can offer some solutions to my problem. I need to prove “boots on ground” to receive disability benefits for Diabetes Mellitus II, Kidney Failure, Hypertension, Left Leg Above Knee Amputation and individual unemployability. VA has denied both disability claims because of no official documentation. In 1972 I was an 18-year-old kid, fresh out of High School, Boot Camp and MMA School and sent to fleet. I had orders to USS Haleakala on station off the coast of Vietnam. There are 34 unaccounted days after reporting off leave at Naval Station Pearl Harbor on April 27, 1972 and reporting for duty aboard USS Haleakala (AE-25) on May 29, 1972. An 18-year-old US Navy sailor can’t disappear in Southeast Asia and magically appear 34 days later on the pier in Subic Bay, Philippines. I have completed the missing information with my personal recollections. Listed below are facts about the 34 missing days: 1. I was never arrested for AWOL, Missing Ships Movement or Desertion during the unaccounted 34 days. 2. I didn’t own a passport and was traveling under official US Navy orders. The United States was at war with Vietnam. It was common practice for Navy personnel reporting to a ship on station to transit through Da Nang. I arrived Da Nang, Vietnam aboard a MAC flight and transferred to a US Navy ship. Stepping off the MAC flight onto the tarmac substantiates “boots on ground”. 3. On April 18, 1972 I departed Machinist Mate A School at Naval Station Great Lakes, Illinois on ten days leave in Honolulu, Hawaii. 4. On April 27, 1972 I reported off leave at Naval Station Pearl Harbor, Hawaii; and departed Honolulu, Hawaii aboard an 8-hour MAC flight enroute to Yokota, Japan. On April 28, 1972 I departed Yokota, Japan aboard a 5-hour MAC flight enroute to Da Nang, Vietnam. On arrival in Da Nang, Vietnam, I disembarked plane, walked across the tarmac to US Customs inside the terminal. After customs, I boarded a bus outside the terminal to the pier and reported TDY aboard the USS Samuel Gompers (AD-37). 5. On April 30, 1972 the USS Samuel Gompers (AD-37) departed Da Nang, Vietnam for Naval Station Subic Bay, Philippines. 6. US Navy paid me aboard USS Gompers on April 30 and May 15, 1972. 7. On May 29, 1972 I reported for permanent duty aboard USS Haleakala (AE-25) at Subic Bay Naval Base, Philippines. Here is the problem: No documentation exists proving the above information. No official orders exist in my service file. No US Customs documentation exists for Yokota or Da Nang. No MAC flights manifests exist. No documentation of TDY service aboard USS Gompers exists. No financial pay records exist. I would appreciate any advice you can offer.
  9. The BVA remanded my claim back to VARO, two years ago. The remand order was for VARO to develop and adjudicate my claim, well about a year ago they did adjudicate my hypertension, and about six months ago I had C & P Exams done for my kidney and sleep apnea, so I contact the VARO in June 2016, and reminded them that my remand was about 2 years old, and when were you all going to finish adjudicating it, so they told me, we're trying to get everything together here very shortly. So a month after that, I received a letter in the mail from VARO, stating that we have certified your appeal to the BVA, your records are being transferred to Washington DC. My question is, if the VARO did not adjudicate my kidney disease and sleep apnea, as the BVA remand order clearly stated, aren't the BVA just going to return the claim for those two claim items they fail to adjudicate at the RO. I contact the ro and asked them why didn't they adjudicate the kidney and sleep apnea before returning it to BVA, one of the supervisors over there inform me that we cannot talk about the claim because we no longer have it, I would need to contact BVA if I had any questions.
  10. Has anyone had any luck with claiming Sleep Apnea as secondary to Hypertension and/or Arteriosclerotic Heart Disease ? My husband has service connection for both hypertension and heart disease and now a current diagnosis and medical equipment for sleep apnea. I've read where VA has approved hypertension secondary to sleep apnea and heart disease secondary to sleep apnea, but not the other way around. If anyone has an archived VA citation in this regard, or personal experience, would greatly appreciate hearing about it. Thanks all.
  11. Received a letter from BVA today stating all 3 of my claims have been granted. I filed for bilateral peripheral vascular disease, carotid artery disease & hypertension secondary to PTSD in Spring 2010 - 5 1/2 yrs ago. Can anybody tell me how the bilateral carotid artery disease will be rated? I've found all of the information I need regarding PVD & hypertension. Also, when I filed all of my appointments to monitor my PVD were dropped so I'm assuming they will order testing before rating...Am I correct on this? Thank you for any words of wisdom you can give me. CHR49
  12. With the hopeful resolve of most AO IHD claims in the next few months-I wanted to get this info posted here again. And to remind all- if their claim comes under Nehmer and they have contacted NVLSP, I have posted the link here many times, please contact NVLSP again to let them know of the decision. "According to Harrison's Principles of Internal Medicine (Harrison's Online, Chapter 237, Ischemic Heart Disease, 2008), IHD is a condition in which there is an inadequate supply of blood and oxygen to a portion of the myocardium; it typically occurs when there is an imbalance between myocardial oxygen supply and demand. Therefore, for purposes of this regulation, the term ``IHD'' includes, but is not limited to, acute, subacute, and old myocardial infarction; atherosclerotic cardiovascular disease including coronary artery disease (including coronary spasm) and coronary bypass surgery; and stable, unstable and Prinzmetal's angina. Since the term refers only to heart disease, it does not include hypertension or peripheral manifestations of arteriosclerosis such as peripheral vascular disease or stroke. http://www.regulatio...A-2010-VBA-0005" (Of course if IHD has caused stroke or any other secondary condition, those conditions should be claimed as secondary to the IHD and will need medical evidence of the nexus of the claimed secondary to the IHD. ) VA will be using 38 CFR$ 4.104 to rate the AO IHD claims. They will be using either diagnostic code 7005 0r 7006 "7005 Arteriosclerotic heart disease (Coronary artery disease): With documented coronary artery disease resulting in: Chronic congestive heart failure, or; workload of 3 METs or less results in dyspnea, fatigue, angina, dizziness, or syncope, or; left ventricular dysfunction with an ejection fraction of less than 30 percent 100 More than one episode of acute congestive heart failure in the past year, or; workload of greater than 3 METs but not greater than 5 METs results in dyspnea, fatigue, angina, dizziness, or syncope, or; left ventricular dysfunction with an ejection fraction of 30 to 50 percent 60 Workload of greater than 5 METs but not greater than 7 METs results in dyspnea, fatigue, angina, dizziness, or syncope, or; evidence of cardiac hypertrophy or dilatation on electrocardiogram, echocardiogram, or X-ray 30 Workload of greater than 7 METs but not greater than 10 METs results in dyspnea, fatigue, angina, dizziness, or syncope, or; continuous medication required 10 7006 Myocardial infarction: During and for three months following myocardial infarction, documented by laboratory tests 100 Thereafter: With history of documented myocardial infarction, resulting in: Chronic congestive heart failure, or; workload of 3 METs or less results in dyspnea, fatigue, angina, dizziness, or syncope, or; left ventricular dysfunction with an ejection fraction of less than 30 percent 100 More than one episode of acute congestive heart failure in the past year, or; workload of greater than 3 METs but not greater than 5 METs results in dyspnea, fatigue, angina, dizziness, or syncope, or; left ventricular dysfunction with an ejection fraction of 30 to 50 percent 60 Workload of greater than 5 METs but not greater than 7 METs results in dyspnea, fatigue, angina, dizziness, or syncope, or; evidence of cardiac hypertrophy or dilatation on electrocardiogram, echocardiogram, or X-ray 30 Workload of greater than 7 METs but not greater than 10 METs results in dyspnea, fatigue, angina, dizziness, or syncope, or; continuous medication required 10 VA Schedule of Ratings.
  13. All, Just was looking at my disabilities on eBenefits. In 2016 I did a new claim for heart disease as I was service connected for hypertension in 2008 and after a lot of reading and looking at my old med records it appeared to me that I probably had heart disease back in 08 and should have claimed it then but I was just a Soldier back then and not a doctor like I pretend to be know. LOL. Here is what is posted regards my heart in eBenefits currently; hypertension..................................................................................................................................0% Service Connedted 08/19/2008 >tricuspid regurgitation (also claimed as heart disease).................................................................Not Service Connected >hypertensive heart disease (also claimed as concentric left ventricular hypertrophy).................30% Service Connected 05/10/2016 Now in my med records I have/had evidence of LVH (enlarged left ventricle) and subsequenlty was granted the 30% secondary to HBP accordingly. Now also in my med records was tricuspid regurgitation on at least 3 ECG's from active service. Now my question is not that I think I should get more comp for the tricuspid regurgitation, as probably the heart disease trumps that, but why not Service Connected at 0%. I don't understand the "Not Service Connected". Seems the same evidence proves both? My hypertension is SC'd at 0% because it is controlled by meds which is correct. FWIW. Anyway, just wondering, Hamslice
  14. Hi everyone. I have a question regarding tinnitus. I filed last year and was denied without a C&P exam. I spent most of my career on the admin side due to what civilians call medical malpractice at an Air Force hospital. So, other than a short tour in Bosnia, no combat experience that could have caused it. I would like to know if tinnitus could be secondary to one of my other disabilities. Please don't get me wrong, I don't want anything I'm not entitled to, but I've had ringing in my ears for as long as I can remember so if it is service connected, I'd like the VA to rate it. I am currently rated for: MDD-70% Sleep Apnea-50% Sciatica, Right-40% BPH-40% Tracheotomy Scar-30% (this, and everything related to it, is where they really screwed me up) Sciatica, Left-20% right medial epicondylitis-10% GERD-10% Allergic Rhinitis-10% Sinusitis-10% (secondary to rhinitis) Deviated Septum-10% Hypertension-0% Left thumb scar-0% Meds currently include Divalproex, Bupropion, Lisinopril/HCTZ, Nexuim, Atorvastatin, Hydroxyzine Pamoate, and Tamulosin. I apologize for the length of this. Like I said, if tinnitus isn't tied to any of this, fine. But if it is, I'd like that service connection documented. Thanks everyone.
  15. I just had two C&P exams this morning and am trying to keep a positive mindset, but the glass looks half empty to me. Maybe someone else can offer some insight on my situation. Since April, I have been rated at 60%; 50% for PTSD and 10% for tinnitus. The claims process for those went pretty smoothly, really, and I was awarded my disability ratings in very short time. I have since then filed three additional claims. My intent to file was back in April, but I submitted the claims on July 25. These three claims are for hypertension secondary to PTSD, sleep apnea secondary to PTSD and for hearing loss. Today I had my C&P exams for the hearing loss and hypertension. I have heard nothing about scheduling a C&P for the sleep apnea. My first exam this morning was for hypertension. I was diagnosed with hypertension, by a private doctor, about 4 years ago and have been on medication since then and am currently being treated by the VA for my hypertension. My hypertension isn't very severe, but it is outside of normal parameters and has been this way consistently for quite a few years. Even though I wasn't officially diagnosed until 2013, I have (and submitted) evidence of prior medical records that show high blood pressure readings well before my actual diagnosis. I don't think I meet the criteria for anything more than a 0% rating, but that's all I really want, or need. I believe I have bradycardia (abnormally low pulse), as a result of my high blood pressure. My blood pressure has always fluctuated and spiked in relation to my PTSD symptoms, so I certainly think the PTSD aggravates my blood pressure, but I don't feel good about my C&P exam from this morning. The doctor was one of the weirdest people I've come across at the VA, so it was hard to get a good read on him. All he did was take my blood pressure 3, or maybe 4, times, all from my right arm, while I was seated. He wanted to know when I was first diagnosed and how many times they had taken my blood pressure during the visit in which I was diagnosed. I told him it was in 2013 and, although I didn't recall how many times they took a blood pressure reading, I did remember how high it was when I was diagnosed. I tried to discuss the evidence I had submitted to support my having actually had high blood pressure before my 2013 diagnosis, but he shut me down. He said anything that I sent in with my claim wasn't his concern. All he was doing was "checking the boxes" on my blood pressure exam and someone else would look at everything that was submitted. This doesn't make sense to me. Isn't the purpose of the C&P exam to look at the evidence, as well render an opinion? I have already been diagnosed with hypertension and am receiving treatment. I'm guessing my blood pressure readings from the C&P exam are within normal parameters...that's what the medication is for. I don't understand the point of putting me through this dog and pony show, but I certainly didn't walk out of there feeling good about it. Next, I had my audiology exam for my hearing loss claim. I just had a audiology exam a little less than 2 months ago from a VA contractor and was subsequently issued hearing aids from the VA about a month ago. As I mentioned earlier, I already receive compensation for tinnitus, so part of me feels like the VA has already conceded that I had sufficient noise exposure in-service to cause damage, but I have also heard of people winning on tinnitus and losing on hearing loss. Since I had just recently had an audiology exam, I was only given an abbreviated C&P exam for my hearing. The audiologist stated that the contractor had not "submitted a full report", or something to that effect, so she only needed to do a partial test today. She asked me a little about my in-service noise exposure, as well as about my civilian occupations. It was over pretty quickly. I didn't feel quite as bad, or confused about that one as the hypertension C&P, but both of them seemed rushed and indifferent. When I got home, I logged in to eBenefits to check on something unrelated and decided to look at my claim status. It had gone from Gathering Evidence to Preparation for Decision, since the last time I had checked on it. How could it be in Preparation for Decision? Mind you, I just had two C&P exams a couple of hours before. There is no way those reports had been sent in and considered already, so it had to have moved to Preparation for Decision a day, or more ago. Since I have not been scheduled for a C&P exam for my SA secondary to PTSD, I suspect now that they don't plan to give me an exam for the sleep apnea. The fact that they'd already moved my claim to Preparation for Decision before my exams leaves me with the impression that my claims are doomed to denial. Realistically, both the hypertension and hearing loss should each be rated at 0%, so that won't get me an increase in disability pay anyway, but a positive decision on the SA would. I also need the 0% ones, though, because of their relationship to other problems I have. I'm a little confused by all of this and am certainly not feeling hopeful about my prospects at this point. Am I jumping to conclusion prematurely, or am I making a reasonable conclusion that things aren't going my way? It's been less than 30 days since my claims were filed and it's already been moved to Preparation for Decision before my C&P exams. I don't know what that means, but it doesn't seem good.
  16. I am still awaiting the notification letter with full details but, according to eBenefits, they have denied my claim for hypertension secondary to PTSD. The basis of my claim was not so much that the PTSD caused the hypertension (although I suspect it may have), but that my PTSD aggravates the hypertension. It looks like the decision was based on the C&P examiners opinion that my hypertension is caused by my weight, rather than my PTSD. His notes do not address the issue of the one aggravating the other. I guess I'll appeal the decision, although I'm not sure how that process works, or really what I'll be able to say, or do, differently to help my case. Below is a redacted copy of the C&P exam notes, if anyone would be so kind as to offer an opinion and/or advice. It bears noting that in his remarks, he states that in 2009 I weighed 160 pounds and my blood pressure was normal. However, I thought 140/90 was the upper threshold of normal. The evidence he is citing reflects a reading of 142/86. Does the VA use a different criteria, because 142 is not normal by generally accepted hypertension parameters. Also, he states that the BP readings used to diagnose are not present, but I did the medical records from when I was diagnosed and they show a reading of 150/110 at that time. So, I would have to say that his statement is factually untrue, based on that the evidence that I submitted. --------------------------- Hypertension Disability Benefits Questionnaire Name of patient/Veteran: Shake-N-Bank Is this DBQ being completed in conjunction with a VA 21-2507, C&P Examination Request? [X] Yes [ ] No ACE and Evidence Review ----------------------- Indicate method used to obtain medical information to complete this document: [X] In-person examination Evidence Review --------------- Evidence reviewed (check all that apply): [X] VA e-folder (VBMS or Virtual VA) [X] CPRS 1. Diagnosis ------------ Does the Veteran now have or has he/she ever been diagnosed with hypertension or isolated systolic hypertension based on the following criteria: [X] Yes [ ] No [X] Hypertension ICD code: 00 Date of diagnosis: 2013 2. Medical history ------------------ a. Describe the history (including onset and course) of the Veteran's hypertension condition (brief summary): noted to have high blood pressure and begun on medication on 2013. Had normal pressure in 2009 and weight of 160 pounds. b. Does the Veteran's treatment plan include taking continuous medication for hypertension or isolated systolic hypertension? [X] Yes [ ] No If yes, list only those medications used for the diagnosed conditions: lisinopril c. Was the Veteran's initial diagnosis of hypertension or isolated systolic hypertension confirmed by blood pressure (BP) readings taken 2 or more times on at least 3 different days? [ ] Yes [ ] No [X] Unknown d. Does the Veteran have a history of a diastolic BP elevation to predominantly 100 or more? [ ] Yes [X] No 3. Current blood pressure readings ---------------------------------- Systolic Diastolic Blood pressure reading 1: 138 / 82 Date: 8/23/2017 Blood pressure reading 2: 122 / 78 Date: 8/23/2017 Blood pressure reading 3: 126 / 80 Date: 8/2017 Average Blood Pressure Reading: 128 / 80 4. Other pertinent physical findings, complications, conditions, signs, symptoms and scars ----------------------------------------------------------------------- a. Does the Veteran have any other pertinent physical findings, complications, conditions, signs or symptoms related to the conditions listed in the Diagnosis Section above? [X] Yes [ ] No If yes, describe (brief summary): 8/11/2017 209 lb b. Does the Veteran have any scars (surgical or otherwise) related to any conditions or to the treatment of any conditions listed in the Diagnosis Section above? [ ] Yes [X] No c. Comments, if any: No response provided 5. Functional impact -------------------- Does the Veteran's hypertension or isolated systolic hypertension impact his or her ability to work? [ ] Yes [X] No 6. Remarks, if any ------------------ No remarks provided. **************************************************************************** Medical Opinion Disability Benefits Questionnaire Name of patient/Veteran: Shake-N-Bake ACE and Evidence Review ----------------------- Indicate method used to obtain medical information to complete this document: [X] In-person examination Evidence Review --------------- Evidence reviewed (check all that apply): [X] VA e-folder (VBMS or Virtual VA) [X] CPRS MEDICAL OPINION SUMMARY ----------------------- RESTATEMENT OF REQUESTED OPINION: a. Opinion from general remarks: relation of hypertension to PTSD b. Indicate type of exam for which opinion has been requested: hypertension TYPE OF MEDICAL OPINION PROVIDED: [ MEDICAL OPINION FOR SECONDARY SERVICE CONNECTION ] b. The condition claimed is less likely than not (less than 50% probability) proximately due to or the result of the Veteran's service connected condition. c. Rationale: The pressures used to diagnose hypertension are not available but apparently were there in 2013 when he was started on medication. He has gained nearly 40 pounds of weight since 23009. This is the most likely caused of his hypertension and the PTSD is less likely than not. ************************************************************************* /es/ FRANCIS M REMBERT MD
  17. Can Type II Diabetes be service connected to Hypertension or pain and nerve meds for other service connected injuries? I have gained a lot of weight in the past couple of years due service connected back and sciatic nerve problems that have pretty much made me bed ridden. Can this be considered a secondary condition to any of these issues.
  18. Hello All, I just seen my c&p exam results. I filed for a loss of organ claim secondary to TCE exposure, from working with TCE for 15 years. Had a nexus from wrii exposure VA doctor saying it was at least as likely as not being exposed to TCE for a prolonged period caused it. My two questions. Dr. David Anaise will do an IMO after I send him all that I have on it. Do you think two against one opinion would turn it in my favor and what form or how do you file for reconsideration instead of two year NOD wait? The examiner basically referred to this website below for his diagnosis for least likely statement. I did smoke pack a day and I am 6' 2" 230 pounds. Thank you please refer to scholarly article, https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3012455/ for details. main risk factors for kidney cancer are cigarette smoking, obesity and hypertension. veteran has history of smoking cigarette, and also has obesity. currently there is no evidence that exposures to chemicals including trichlorethylene and other solvents cause or aggravate kidney cancer. the author concluded tghat " casual conclusions are not yet supported " and that " Genetic susceptibility and its interaction with environmental exposures are believed to influence renal cell cancer risk, but limited studies based on candidate gene approaches have not produced conclusive results." therefore, to answer question asked, veteran's kidney cancer is LESS likely related to military service; as there is no definitive evidence that exposures during service caused or aggravated the kidney cancer.
  19. Hello,I am filing for presumptive SC for hypertension; working with VSO and my readings and diagnosis fit within the criteria for disabling (at least 10%) within 1 year of discharge from active duty, but the medical opinion from my c&p states there is no "direct service connection". Has anyone experienced this before? Will the VSR ask for another medical opinion based on presumptive SC or is this how the medical opinions are always worded regardless? Here is verbiage directly from the physician's medical opinion strictly for hypertension: SC:MEDICAL OPINION SUMMARY-----------------------RESTATEMENT OF REQUESTED OPINION: a. Opinion from general remarks: Veteran claims hypertension due to illness or event on active duty b. Indicate type of exam for which opinion has been requested: hypertensionTYPE OF MEDICAL OPINION PROVIDED: [ MEDICAL OPINION FOR DIRECT SERVICECONNECTION ] b. The condition claimed was less likely than not (less than 50%probability) incurred in or caused by the claimed in-service injury, event or illness. c. Rationale: Review of the STR shows no evidence of the diagnosis ortreatment for hypertension while on a period of active duty. The veteranwasdiagnosed in December 2004 with CHF due to valvular heart disease along with hypertension. MEDICAL OPINION SUMMARY-----------------------RESTATEMENT OF REQUESTED OPINION:a. Opinion from general remarks: Veteran claims hypertension due to illness or event on active dutyb. Indicate type of exam for which opinion has been requested: hypertension TYPE OF MEDICAL OPINION PROVIDED: [ MEDICAL OPINION FOR DIRECT SERVICE CONNECTION ]b. The condition claimed was less likely than not (less than 50% probability) incurred in or caused by the claimed in-service injury, event or illness.c. Rationale: Review of the STR shows no evidence of the diagnosis or treatment for hypertension while on a period of active duty. The veteran was diagnosed in December 2004 with CHF due to valvular heart disease along withhypertension.*******************************************************************
  20. I was awarded 10% for hypertension back in 1997 and was taking vasotec 15 mg. However, after incurring a severe heart condition, and I now take verapamil 240 mg er 1/ day and propafenone hydrochloride 325 mg er 2 / day. I have a pacemaker for bradycardia, supraventricular tachychardia, and sss. I gave up filing for the pacemaker. My va rep said he didn't want to deal with it and my doctors won't give me any type of statements to help me out. So, now I will file alone for my meds. The question is..Do I upload my prescriptions on ebenefits.gov under a new claim or should I find a mental hospital and sign in? Don't think i can take much more of this.
  21. Hello All! I was notified that some day I will be receiving a letter to go to Washington for a hearing for my appeal. I filed for hypertension secondary to chronic pain. Here is a synopsis... Leading up to my first surgery in 1994 done by the Army. I was told to come into the aide station to have my blood pressure recorded. Being a dumb 21 year old Airborne Infantryman I didn't think nothing of it. I went, my pressure was high and it was logged in my medical records. I had my spinal fusion to correct a parachuting accident. Mar 1994, I was discharged because the fusion didn't work. Right before, back to the aide station for blood pressure check-ups. I didn't file for it at discharge cause they don't tell you those things then. 1998 I am put on blood pressure medication and an aspirin at the VA hospital in Pittsburgh. 2003 (roughly) I was 31 and I had a mini-stroke. I went to the VA in Pittsburgh, they couldn't find anything. I move to Texas with my Ex and our kids. Shortly there after, I get a call from the Nuerology Department at the VA. You need to see a Neurologist, we found something. I go see one. The is when I found out about the TIA. I the mean time, I did file for Service Connected for Hypertension and was denied. I figured, screw it. I got the rating I was happy with for me back and knees. The EX leaves and I am taking care of my three kids on my own. My blood pressure is not controlled and neither is my pain. I go to the ER on several occasion, without telling the Triage nurse what is wrong she sees my BP is high and says, "you are in pain." At this point, I am put on double the dose of medication. Due to my blood pressure being high from the chronic back and knee pain. Has anyone out there tried to do this and succeeded? I am concerned with the hearing coming up, who knows when, but this has been on my mind to ask. Thank-you all for any and all input! Jim
  22. Hello, Just had my C&P for hypertension and got the exam results. Can someone look at the results and tell me what my rating might be. Thank you. Hypertension Disability Benefits Questionnaire Is this DBQ being completed in conjunction with a VA 21-2507, C&P Examination Request? [X] Yes [ ] No ACE and Evidence Review ----------------------- Indicate method used to obtain medical information to complete this document: [X] In-person examination Evidence Review --------------- Evidence reviewed (check all that apply): [X] VA e-folder (VBMS or Virtual VA) [X] CPRS Evidence Comments: Evidence of elevated BPs dating back to 8/1996 - 123/92; 2000 - 145/82, 152/82, 132/85 2004 - 136/90 2005 - 136/102, 130/90 1. Diagnosis ------------ Does the Veteran now have or has he/she ever been diagnosed with hypertension or isolated systolic hypertension based on the following criteria: [X] Yes [ ] No [X] Hypertension ICD code: XXX Date of diagnosis: 2005??? 2. Medical history ------------------ a. Describe the history (including onset and course) of the Veteran's hypertension condition (brief summary): Veteran reports he has had high blood pressure for a number of years - does not recall specific date b. Does the Veteran's treatment plan include taking continuous medication for hypertension or isolated systolic hypertension? [X] Yes [ ] No If yes, list only those medications used for the diagnosed conditions: Lisinopril 20 mg daily c. Was the Veteran's initial diagnosis of hypertension or isolated systolic hypertension confirmed by blood pressure (BP) readings taken 2 or more times on at least 3 different days? [ ] Yes [ ] No [X] Unknown d. Does the Veteran have a history of a diastolic BP elevation to predominantly 100 or more? [ ] Yes [X] No 3. Current blood pressure readings ---------------------------------- Systolic Diastolic Blood pressure reading 1: 144 / 88 Date: 2/3/2017 Blood pressure reading 2: 157 / 94 Date: 2/3/2017 Blood pressure reading 3: 148 / 91 Date: 2/3/2017 Average Blood Pressure Reading: 149 / 91 4. Other pertinent physical findings, complications, conditions, signs, symptoms and scars ----------------------------------------------------------------------- a. Does the Veteran have any other pertinent physical findings, complications, conditions, signs or symptoms related to the conditions listed in the Diagnosis Section above? [X] Yes [ ] No If yes, describe (brief summary): Veteran reports he will experience headaches when his blood pressure is up; states he grets readings that are higher at home on his machine b. Does the Veteran have any scars (surgical or otherwise) related to any conditions or to the treatment of any conditions listed in the Diagnosis Section above? [ ] Yes [X] No c. Comments, if any: No Side Effects on BP medication 5. Functional impact -------------------- Does the Veteran's hypertension or isolated systolic hypertension impact his or her ability to work? [ ] Yes [X] No 6. Remarks, if any ------------------ Opinion: The Veteran's diagnosis of hypertension is at least as likely as not realted to elevated BPs in active duty service. Rationale: There is evidence of elevated BPs in active military STRs. Veteran reports that he has taken his BP medication today.
  23. I filed a claim for hypertention in april 2015. My claim was denied in Oct.16 stating that it was not sc and no evidence in my medical records. I went through my smr and found over 7 times that my pressure was taking and it read higher than 120 and numerours times in the 140. What should I do now? Any advice is appreciated. Thanks
  24. Is Parkinsonism presumptive as it is in Parkinson's for Viet Nam vets if exposed to herbicides? I recently had a MRI of the head checking for clots. Surprisingly the report came back stating : "MRI head: There is a punctate chronic lacunar infarct of the left caudate head. There is no evidence of hemorrhage, edema, masses, mass effect, midline shift or infarction. The ventricles and sulci are normal in caliber and configuration. Scattered areas of nonspecific periventricular, subcortical and deep white matter T2/FLAIR hyper intensity are in a configuration most suggestive of chronic small vessel ischemic disease. There is no abnormal enhancement after contrast administration. There is no abnormal focus of slowed diffusion. The principal intracranial vascular flow voids are preserved. The dural venous sinuses are patent on MP-RAGE images. " I apparently have some kind of asymptomatic stroke and was not aware of it (lacunar infarct). Also there is the subject of 'white matter' and 'chronic small vessel ischemic disease' Has anyone filed these conditions as secondary? I am SC for IHD, DMII, PTSD. From what I have read the Lacunar Infarct is mostly caused by hypertension.
  25. HI EVERYONE THIS IS MY FIRST POST I DO IN HERE, I AM OIFAND OEF VETERAN, I GOT OUT THE SERVICE IN 2005, I WENT TO THE VA FOR THE FIRST TIME IN 2006, MY PRIMARY DOCTOR DIAGNOSED ME WITH PTSD BACK IN 2006. VA HAS ME AT 80% RATING. I HAD TWO SEPRATE C&P EXAM ONE IN SEPTEMBER 2016 AND ONE ON NOVEMBER 22, 2016, THE ONE FOR SEPTEMBER THE PYSCHIATRIST TOLD ME THAT I HAD PTSD, AND VA SAYS I DONT HAVE PTSD, BUT I WAS FIRST DIAGNOSED IN 2006, SO MY LAST C&P EXAM THE PYSCHIATRIST WROTE ON MY NOTES THAT I HAVE PTSD, MY QUESTION IS WILL I GET A RETRO FROM 2006 OR 2016... bilateral hearing loss 40% unspecified trauma and stressor related disorder with major depressive disorder (previously addressed as major depression) 50% bilateral hearing loss 40% hypertension 10% tinnitus 10%
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