- Temporomandibular Dysfunction Disorder (TMJD)
- Back/Neck Pain
- Complex Regional Pain Syndrome (CRPS)
- Fibromyalgia (FM)
- Peripheral Neuropathy (PN)
- Postherpetic Neuralgia (PHN)
- Vertebral Fractures:
- Sleep Disorders:
- Narcolepsy with or without Cataplexy
- REM sleep behavior disorder (RBD):
- Obstructive Sleep Apnea (OSA)
- Restless Leg Syndrome (RLS)
- Shift Work Disorder (SWD)
Benign Essential Tremor (BET)
BET is an action tremor where the patient experiences tremor while attempting to do a specific action such as writing, eating or drinking. The tremor is typically worse when the patient is anxious and/or in a public gathering and betters when at home or relaxed. The tremor is typically hereditary, running in the family. BET is a disease of its own and completely unrelated to Parkinson disease. It is benign, as the name states and harmless, yet annoying. The diagnosis is based on clinical history and examination. There is no specific test to confirm it nor rule it out. The tremors, however, if there are other associated symptoms, require an MRI of the brain to evaluate for other neurologic disorders.
There is no cure for BET; however, treatment is used to suppress the tremors. Treatment is initiated when the tremors are interfering with the activities of daily living and become embarrassing to the patient. Commonly used medications are Primidone (Mysoline), Propranolol (Inderal) and occasionally Topiramate (Topamax). When tremors are extremely severe and fail medications, the patient might consider deep brain stimulation. We manage and program the deep brain stimulators in our office after a local neurosurgeon implants it.
Carpal Tunnel Syndrome (CTS)
The median nerve starts at the axilla and extends all the way down to the hand entering at the wrist through an area called the carpal tunnel. In CTS the nerve is pinched at that level (wrist). Causes of nerve impingement can be from repetitive use of the wrist (typing), pregnancy, thyroid problems, diabetes, and other disorders.
The typical presentation for CTS is numbness and tingling sensation in the first, second, third and half of the fourth digit, pain at the wrist that shoots up and down the arm. Symptoms are worse at nighttime, often waking up the patient from sleep, requiring the patient to shake off the hands to relieve the symptoms. Weakness in handgrip develops in moderate to sever cases.
The diagnosis of CTS is based on the clinical symptoms and physical examination. However, confirmation is done with a nerve conduction velocities test and electromyography, which localizes the nerve impingement and severity of it.
The treatment of the CTS depends on the severity of the nerve impingement. Mild CTS can be easily treated with the wrist splint or nerve block. Splits should be worn at all times and for several months but, most importantly at night time. In moderate to severe cases surgery to release the nerve might be required to avoid progressive weakness and loss of function.
Concussion and Post-Concussion Syndrome (PCS)
The brain is housed within the skull and surrounded with a thick connective tissue called the dura connecting the brain to the skull. Essentially the brain is hanging and floating within the skull, but tightly stabilized. If a person suffers a direct or indirect blow to the head, from an assault, motor vehicle accident, or a fall, the brain is shaken within the skull. This results in disturbances in the brain at a microscopic level. These disturbances affect the connection between the brain cells and may result in a group of symptoms such as headache, loss of consciousness and/or dizziness.
If the symptoms persist after the injury, then it becomes PCS. Symptoms are vast and can include, headache, dizziness, lightheadedness, vertigo and sleep, memory and mood disturbances. The symptoms can last from days to months. The diagnosis of concussion and PCS is based on the history and clinical picture since imaging and other diagnostic modalities are usually unremarkable.
The treatment of concussion and PCS is supportive; done by treating the symptoms. Medications can be used to treat headaches, insomnia or other symptoms. Social support is essential in the treatment and reassurance that the symptoms are not going to last indefinitely and will slowly improve.
Dementia is a cognitive dysfunction in which memory, attention span, and problem solving are affected. The most common types of dementia are Alzheimer’s disease (AD); however, other types include multi-infarct dementia, Lewy-body dementia, Pick’s disease, alcohol related dementia, and other unusual types.
AD results from the degeneration of the nerve cells and the deposit of specific proteins within the brain cells. The typical presentation is slowly progressive loss in memory, problem solving, and cognitive dysfunction. The patient is noticed to forget names of close family members, repeating themselves, forgetting doing things they have done a few minutes earlier, getting lost driving, inability to balance checkbook and other symptoms.
The diagnosis of AD is based on the clinical presentation; however, tests are done to rule out any other diseases that mimic AD. Typical workup includes MRI, metabolic workup (blood work) and possible EEG. It essential to rule out and diagnose other than AD.
There are two classes of medications approved for AD; acetylcholine esterase inhibitors (Aricept and Exelon) and glutamate receptor modulator (Namenda) or the newer combination medication of Aricept and Namenda (Namzaric). In addition, B vitamins can be helpful such as Cerefolin with NAC or over-the-counter B complex. These medications do not produce an immediate effect from day to day but instead, they slow down the progression of the disease over the years. Family education about AD and counseling is essential in managing the patient.
AD can also have associated sequelae or symptoms in addition to the memory including agitation, delusions, insomnia, and/or sleep disorders. These conditions are treated accordingly.
When patient presents with dizziness, the initial step is to differentiate if the symptom is lightheadedness or vertigo. Lightheadedness is the feeling as if you might faint. Your body may feel heavy while your head feels as if it is not getting enough blood. Vertigo is the sensation of a whirling, spinning sensation and loss of balance. It is essential to differentiate between the two since the evaluation and treatment is different. Lightheadedness is most likely related to cardiac etiology or blood pressure changes. Vertigo on the other hand is neurologic and related to vestibular dysfunction. If it is lightheadedness, we try to assess for heart and/or blood pressure problems or medication side effects.
Vertigo is divided into peripheral and central. Peripheral vertigo is caused by a dysfunction in the vestibular system outside the brain (inner ear). There are three tubes in the inner ear containing fluid and hair cells that control balance. Any problem within these tubes such as infection, inflammation or calcium particles causes vertigo. Based on the history and physical examination, we are able to determine the etiology of this type of vertigo. Examples of peripheral vertigo syndromes include, benign positional vertigo, vestibular neuritis and Meniere’s syndrome. Each has specific presentation that differentiates it from the others. Treatment of the peripheral vertigo depends on the etiology. This can include medications to suppress the vertigo and specific exercises (Epley Maneuver) that can improve the symptoms.
Central vertigo involves the vestibular system that is within the brain. Causes of central vertigo include stroke, multiple sclerosis, infection and masses/tumors. Typically, central vertigo is associated with other symptoms such as unsteadiness or gait disturbances, numbness, tingling sensation, visual changes, and/or weakness. Central vertigo is more serious and requires immediate action and treatment. Workup for central vertigo must include, but not limited to MRI and MRA of the brain, possibly carotid ultrasound. Treatment depends on the cause.
In our office, we provide vestibular rehabilitation where there is specific equipment to help desensitize the vestibular system, thus helping in improve symptoms dramatically.
Migraine headaches are a specific type of headaches, which are caused by a group of nerve cells at the base of the brain producing chemicals that affect blood vessels causing them to be inflamed and dilate producing the headache. The headache is typically described as a throbbing, pulsating, commonly on one side of the headache and typically associated with sensitivity to light and noise, nausea, and vomiting. However, migraine headache can have any presentation and can involve the entire head.
The two major types of migraine headaches are the common and classic migraines. Classic migraine is usually preceded by an aura (a group of symptoms [commonly visual] that precede the headache). The typical visual changes patients describe are flashes of light, zigzag lines, floaters, and occasionally tunnel vision. The aura is felt minutes or several hours before the headache onset. Common migraine is not preceded by an aura. However, the headache symptoms are the same as the classic one.
There are also different types of unusual migraines such as complex migraine where the patient experiences stroke like symptoms (numbness, tingling sensation, weakness, and slurred speech). Another is basilar migraine, where the basilar artery is involved (at the base of the brain) producing unique symptoms including: dizziness, vertigo, nausea, vomiting, altered mental status, gait disturbance and other symptoms. Other unusual migraine syndromes include cyclic vomiting (periodic vomiting without the headache) that is usually in pediatrics. Ocular migraine presents with visual changes without headache either.
Migraine headaches are more common in females. Although there is no genetic link identified, it typically run in families. It can involve patients at any age; however, it is common amongst ages 20 to 30. In certain cases, migraine headaches can present as early as two years of age.
There are two types of treatment for migraine headache: abortive therapy and prophylactic therapy.
In abortive therapy, the focus is on giving a medication that stops the migraine attack. The classic class of medications used for abortive therapy is the Triptans including Imitrex, Maxalt, Zomig, Relpax, Axert, and Treximet (in tablets, melting tablets, nasal spray or injections). Other abortive therapies include Acetaminophen, Ibuprofen, Naproxen, butalbital with or without codeine and Aspirin. The key in aborting migraine headaches is to take the medication early at the onset of the headache. The longer the patient waits to take the medication, the more difficult it is to stop it.
Migraine prophylactic therapy is a medication that is taken on daily basis to prevent the headache. It decreases the intensity and frequency of the headaches. The typical recommendation for taking prophylactic therapy is for patients with more than three headaches a month, a headache that lasts more than 24 hours, headache that causes deficits (as complex migraine) or a headache that interferes with the activities of daily living.
Common prophylactic medications for migraine headaches include Topiramate, Propranolol, nortriptyline, amitriptyline, Cymbalta, Effexor, Lyrica, Neurontin, and Keppra.
Interventional procedures are also used to treat migraine headaches. These include sphenopalatine ganglion block, occipital nerve block, dorsal median branch block of the upper cervical spine followed by radiofrequency, stellate ganglion block, and/or Botox injection. We have had good success with electrical anesthesia where small pads are placed in the back of the head over the occipital nerves and we send high frequency electrical impulses to stimulate the occipital nerves.
Multiple Sclerosis (MS)
MS is a central degenerative (demyelinating) disease that involves the myelin sheaths (covering) surrounding the nerve fibers in the brain or the spinal cord. It is classified as an autoimmune disease where the autoimmune system produces antibodies that attack the nerve fibers.
Typically, it is more common in females, and more common in the northern hemispheric population. The typical presentation for MS is dependent on the area of the brain or the spinal cord that is affected and last more than 24 hours and include a numbness and tingling sensation of one side of the body or one limb, weakness, double vision, painful loss of vision (optic neuritis) and if it involves the spinal cord, it can affect the urination and both sides of the body.
There are several types of MS including relapsing remitting (most common), primary progressive and secondary progressive. The difference between these types is the presentation and the progression; treatment can also vary.
The diagnosis of MS is done with MRI of the brain and/or spinal cord with contrast, lumbar puncture to check for specific markers in the cerebral spinal fluid and occasionally evoked visual and/or auditory potential.
Treatment of MS is two folds; acute and maintenance therapies. Treatment of acute attacks involves the use of intravenous steroids. The maintenance treatment involves the use of immune-modulators such as Betaseron, Avonex, Rebif, and Copaxone. Newer oral medications include Gilenya (fingolimod), Tecfidera (dimethyl fumarate), and Aubagio (teriflunomide), other medications include Tysabri (natalizumab). These medications reduce the number of relapses (attacks) and some reduce disability. Supportive care includes physical and occupational therapy, social support and other comorbidities.
Parkinson’s Disease (PD)
PD is a movement disorder where dopamine-producing brain cells die off in a specific area of the brain. Dopamine is responsible for the fluidity of movements. Typical symptoms of PD are resting tremors, shuffling gait, stooped forward, decreased arm swing, decreased turning, slowness (where they are having difficulty turning in bed, getting out of bed, getting out of a chair), and masked faces (where the patient loses the normal expression that people have using their faces). The symptoms are very slowly progressing, occurring over years.
The diagnosis of PD is based on the clinical symptoms and physical examination; there is no specific test to confirm it. However, some testing is done such as MRI and metabolic work up to rule out other disorders that can mimic PD.
It is also important to differentiate PD from Parkinson plus syndromes. These syndromes can in addition to the typical PD symptoms present with other symptoms such as dementia as in Lewy-Body Dementia or autonomic dysfunction (dizziness or orthostatic hypotension) as in multisystem atrophy. Other rare Parkinson plus syndromes also exist.
There is no cure for PD; however, there are medications that can help improve the symptoms, function and the quality of life. These medications include dopamine agonists (Mirapex and Requip), carbidopa-levedopa-entacapone (Sinemet, Stalevo) and also Azilect. These medications typically improve the symptoms and the functionality of the patient; however, it is a delicate balance because certain medications have significant side effects that can be worse than the disease itself.
Other modalities include physical and occupational therapy that improve the patient’s quality of life and activity of daily living. We identify and treat sleep disorders (common in patients with PD). Patient’s family education, is essential in copping with the disease. If symptoms become very severe or patients become resistant to medication, deep brain stimulation implant, done by a local neurosurgeon and programed and maintained at our institute is considered too. We provide the programing and follow-up for those patients.
There are two types of strokes:
Hemorrhagic stroke occurs when a blood vessel within an area of the brain bursts and blood flows into that area. This can be from uncontrolled hypertension, aneurysm, trauma and other rare causes. The treatment is limited for the hemorrhagic stroke depending on the cause. However, this is a medical emergency that needs to be treated in the hospital.
Ischemic strokes can be thrombotic or embolic. A thrombotic stoke occurs when a blood vessel clogs locally within the area of the brain. An embolic stroke on the other hand, occurs when a blood clot breaks off a distal location, such as the heart, the aorta, or the carotids and migrates into the brain. With either type; when blood supply stops to reach an area of the brain a stroke occurs.
Stroke symptoms include, but not limited to weakness, numbness, tingling (of one side of the body or a limb), double vision, gait disturbance, speech disturbance, altered mental status and many other symptoms. In hemorrhagic stroke, headache is very common and the onset is much quicker.
The treatment of ischemic stroke comprises of two components; acute and preventative. In acute treatment, it is essential that the patient reaches the hospital within three hours from the onset of the symptoms; this allows the administration of tissue plasminogen activator (tPA) or “a clot buster” (must be given within three hours from the onset of the symptom) and can result in better outcomes. If the patient does not qualify for this medication, Aspirin, Plavix, or Aggrenox can be used. In embolic strokes Coumadin (warfarin), Pradaxa (dabigatran), Xarelto (rivaroxaban), and Eliquis (apixaban) maybe used. A stroke patient is typically admitted to the hospital to observe and do further testing and treatment. Depending on the symptoms, the patient may need physical, occupational and/or speech therapy.
Stroke risk factors are divided into modifiable and non-modifiable risks. The non-modifiable risks include age above 50, family history of strokes, and male gender. Modifiable risks are hypertension, diabetes, hypercholesterolemia, smoking, carotid artery disease, coagulopathies, atrial fibrillation, and obstructive sleep apnea. The focus of our practice is to prevent strokes by correcting or treating these modifiable risks. Smoking cessation is the most important of all risks since it increases risk of stroke by five folds; it is the cheapest and most effective way to prevent strokes.
We follow up with each patient after returning from the hospital to assess whether additional therapies are required such as physical, occupational, and/or speech therapy. Our goal is to do everything possible to bring that patient fully back to health and normal routine life.
Syncope is the sudden loss of consciousness. When we evaluate the patient for syncope, typically we try to break it down into two categories: cardiogenic or neurogenic. Cardiogenic syncope is typically preceded by lightheadedness, chest pain, palpitation, shortness of breath, and sweating. Typically, it occurs when a patient changes position from a laying down or seated position to standing or in the shower or bathroom. After the patient wakes up typically he/she are back to normal without confusion or disorientation. Neurogenic syncope on the other hand is not preceded by symptoms or occasionally preceded by funny feeling in the stomach, odd sensation in the head, or nausea. It can occur in any position. After the patient wakes up, he/she might be confused, disoriented, with evidence of tongue biting, and loss of bladder or bowel control. They usually feel very tired and sleep for a long period to time afterword.
As neurologists we approach patients with syncope by first determining if it is cardiogenic or neurogenic and do the neurologic workup. Cardiac workup is typically deferred to the cardiologist. Workup may include imaging of the brain (a CAT scan or an MRI), echocardiogram, Electrocardiogram (ECG), carotid ultrasound, electroencephalogram (EEG) and/or (autonomic nervous system (ANS) testing. If there is a suspicion for cardiac etiology, the patient will be referred to a cardiologist to complete the cardiac workup.
The treatment of syncope depends on the etiology. If seizure is proven or strongly suspected, antiepileptic’s are initiated. If dysautonomia is suspected, we try to identify the cause and treat it. If cardiac etiology is suspected, the patient is referred to a cardiologist for treatment.
Acute pain is a sudden pain that can be secondary to trauma, surgery or acute pathology. Acute pain is usually approached aggressively and quickly due to the severity of the pain. Diagnosis and treatment of acute pain depends on the cause. Pain from trauma depends on the mechanism of injury and the affected part. Injury can cause muscle sprain/strain, fracture, ligament pull and/or internal organ injury. Post surgical acute pain also approached differently.
Acute pain can be treated with anti-inflammatories (avoided with bone fractures), muscle relaxants (if muscles are involved), opioids, physical therapy, TENS unit, and durable medical equipment (braces, splints). Interventional procedure that can be used for this type of pain is trigger point injections, facet injections, epidurals, and/or nerve blocks.
The key in treating acute pain is to identify the stressor and remove it. Another focus is to treat the pain quick to prevent it from becoming chronic.
Arthritis pain can be divided into two categories, non-inflammatory such as osteoarthritis and an inflammatory such as rheumatoid arthritis, gout, psoriatic arthritis, lupus and other connective tissue disease. Osteoarthritis typically results from wear and tear within the joint involving the large and small joints such as the ankle, the knee, and/or the hand joints. This pain is conservatively treated with NSAIDs such as Celebrex, ibuprofen, naproxen, meloxicam, or diclofenac. Topical creams/gel can also be used such as diclofenac gel or liquid (Voltaren and Pennsaid) or other compounding creams. If the patient continues to experience pain despite this treatment, then tramadol has been shown to be effective in treating this type of pain. If all fails opioids can be used. Interventional procedures such as steroid injections and/or hyaluronic acid and regenerative medicine can also be used at any point.
Inflammatory arthritis is more difficult to treat is treated in two parallel ways. One way is to treat the disease itself and that is usually managed by a rheumatologist (arthritis specialist) with infusions and other immunosuppressant’s. The other way is to treat the pain associated with it which managed by the pain specialist. This type of pain is treated as osteoarthritis pain outlined above.
Temporomandibular Dysfunction Disorder (TMJD)
The TMJ is the joint that connects the jaw to the skull. This joint is involved in the movement of the jaw chewing, speaking, and other functions. The typical pain that the patients describe with TMJD is a deep aching, nagging pain that can radiate into the ear or down the jaw triggered by chewing or pressure over that joint. Since this is considered an arthritic type of pain, the best approach for it is to use a mouth guard fitted by a dentist. Medications that can be used in treating the pain include NSAIDs (Motrin, ibuprofen, naproxen, meloxicam, diclofenac), tramadol and opioids. Cortisone injections in the joint can be effective in certain patients.
When evaluating patients for back pain, first we assess if the pain is acute or chronic in nature. Acute pain typically is due to trauma, pathologic (tumor, osteoporosis fracture) or overuse of the back area. Chronic pain is typically pain that lasts for several months and persists despite treatment. The next step in approaching patients with back pain is identifying what we call “the pain generator”; the source of pain. Common pain generators in the back are muscles, facet joints, discs, SI joint, ligament, vertebral fracture, tumor/mass and/or referred visceral pain. Identifying the pain generator is essential since treatment is different for each pain generator.
Diagnosing back pain can be accomplished by history, physical examination, imaging (X-ray, CT scan, MRI) and/or nerve conduction study. These tests are essential to characterize the pain before treating it.
Clinical presentation of back pain differs based on the affected area that generates the pain. Muscle pain is described as cramps and spasms involving the muscle itself and can radiate around the affected area. Facet pain is produced by instability and/or arthritis of the facet joints, which are small joints in the back of the spine that allows mobility and stability of the spine. Facet pain is described as deep aching nagging pain that is localized to the affected spine area back that is a lot worse with sitting, standing and activity and improves with laying down.
Disc pain is caused by herniation; a tear or bulging of the disc and at times pushes on the nerve root. Typically, pain is described as back or neck pain, that is deep aching and at times sharp radiating down one or more extremities. It can be associated with numbness, tingling sensations and/or weakness in that extremity. Pain is usually worse in the morning when waking up or laying down and better when leaning forward.
The sacroiliac (SI) joint is a large joint that forms between the sacrum (the base of the spine) and the pelvic bone. It is usually held together with large ligaments and tissue. Any instability in the back or gait can result in pain generated from this joint. Typical SI pain is described as a deep aching and at times burning pain over the buttocks that is a lot worse when standing and walking and better when sitting and laying down. The pain at times can radiate into the groin area, down the buttocks area, but rarely below the knees.
Other back pain generators such as vertebral fractures usually present acutely and are very severe and not affected by position.
Treatment of back pain is dependent on the pain generator. Muscle pain (spasms) is treated with muscle relaxants, trigger point injections, physical therapy, and/or a TENS unit. Facet pain responds better to anti-inflammatories, opiates, physical therapy, facet cortisone injections and/or dorsal median branch block (a very small nerve that supplies each facet joint) and radiofrequency. Disc pain can be treated with anti-inflammatories, opioids, certain antidepressants and anticonvulsants, epidural steroid injections, spinal cord stimulator and/or surgery. SI joint pain can be difficult to treat with medications, however anti-inflammatories and opioids can be used. Steroid injections into the joint and nerve block with radiofrequency are very effective in treating this pain.
Complex Regional Pain Syndrome (CRPS)
CRPS is a chronic neuropathic pain disorder that can result from direct or indirect injury to the nerve. Typically, it involves one limb; however, can spread to involve multiple limbs. The pain is usually described as a severe, lancinating, electric-like, associated with hypersensitivity to touch, changes in skin color, sweating (or lack of) and/or swelling of the involved extremity. Typically, it starts after direct or indirect trauma to the involved nerve.
The diagnosis of CRPS is based predominantly on the clinical presentation, symptoms and clinical examination. Testing is done predominately to rule out any other diagnoses that can mimic CRPS including a nerve conduction test and electromyography, x-ray, an MRI, and bone scan.
The treatment of CRPS can be very difficult due to the severity and the complexity of the symptoms. Multiple medications can be used including anticonvulsants (Lyrica, Neurontin, Trileptal), antidepressants (Cymbalta, Nortriptyline, Amitriptyline, Effexor), tramadol and opiates. Interventional procedures can also help in treating pain associated with CRPS including nerve blocks, epidurals, sympathetic blocks, spinal cord stimulator, and/or intrathecal pump.
FM is a musculoskeletal pain syndrome, more common in females, where patients experience generalized muscle pain, with several trigger points throughout the body.
There is no specific test to diagnose FM. Diagnosis is based on the clinical presentation and physical examination. Tests (blood tests, imaging, etc..) however, are done to rule out other disorders that can mimic FM.
Available treatment for FM include antidepressants (Cymbalta, nortriptyline, Savella) and anticonvulsants (Lyrica, Neurontin). Furthermore, patients might benefit from muscle relaxants (Zanaflex, baclofen), tramadol and opioids and interventional procedures (trigger point injections).
Peripheral Neuropathy (PN)
Peripheral neuropathy (PN) means damaged nerves in the extremities. PN has multiple causes; the main one is diabetes. Other causes include inflammatory disorders (lupus, sarcoidosis, vasculitis,) autoimmune disorders (Guillain-Barre syndrome, chronic inflammatory demyelinating polyneuropathy (CIDP), infectious diseases (HIV, Hepatitis C), B12 deficiency and many other causes.
Patient with PN present with numbness, tingling sensation and burning pain starting in the feet and progresses in an ascending way up the legs and into the arms. When PN progresses, it can cause weakness in the extremities; a gait disturbance, increase falls and reduction in wound healing.
Diagnosing PN includes good history and physical examination, nerve conduction study and an electromyography, metabolic work up (blood test) and/or nerve biopsy.
Treatment of PN has two folds. One is to identify the cause and see if it can be treated and corrected and another to treat the pain and other symptoms associated with it. Treating the cause depends on the cause. Treating the pain and paresthesia can be with anticonvulsants (Neurontin, Lyrica, Trileptal), antidepressants (Cymbalta, nortriptyline), opiates, tramadol, lidocaine patches, topical creams, and interventional procedures (sympathetic blocks, epidural injections and/or spinal cord stimulators). Furthermore, we also have other new modalities such as electrical anesthesia and the builder that can help improve the pain and the feeling in the extremities.
Postherpetic Neuralgia (PHN)
PHN is a chronic neuropathic pain disorder that develops after herpes simplex virus infection (shingles). Typically, starts after the shingles resolves and the pain can persist indefinitely. The pain is described as severe burning pain associated with a numbness and tingling sensation and hyperesthesia (hypersensitivity) over the affected nerve. Typically, the pain presents in the distribution of a dermatome over the affected (the nerve distribution) area.
The diagnosis of PHN is based on the history and clinical examination. There is no specific diagnostic test for it. Treatment can be difficult due to the severity of the pain. Initial approach is the use of anticonvulsants (Lyrica, Neurontin, Trileptal), antidepressants (Cymbalta, Nortriptyline, Amitriptyline, Effexor), tramadol and opiates. Topical creams, gels and patches can be very helpful. Interventional procedures can also help in treating pain associated with PHN and may include nerve blocks, epidurals, sympathetic blocks, a spinal cord stimulator, and/or intrathecal pump.
Vertebral fractures can be very painful. They can be due to either trauma, osteoporosis or a pathological process invading the vertebral body such as cancer or infection. Vertebral fracture causes severe pain, described as a deep aching, nagging, pain that is localized over the affected vertebral body. The pain is constant but might be worse with sitting, standing and activity.
The diagnosis of vertebral fracture is usually accomplished with imaging of the spine, such as X-ray, CAT scan, bone scan and/or MRI.
Treatment can be conservative with back brace, rest, pain medications, interventional procedures such as vertebroplasty/kyphoplasty (injecting cement within the vertebral body) and/or surgery. Vertebroplasty/kyphoplasty can result into immediate and significant relief of the pain and stabilization of the vertebral body. If there is any residual pain after the vertebroplasty/kyphoplasty, a nerve block and radiofrequency around that vertebral body can be done to get more pain relief.
Hypersomnia is defined as excessive daytime sleepiness and can be secondary or primary. Secondary hypersomnia is usually due to something else such as medications, hormonal imbalance, and medical and/or psychiatric disorders. Primary hypersomnia on the other hand is a disorder of its own and no cause can be identified.
The diagnosis of hypersomnia begins with history and the examination and metabolic workup. Some patients might require imaging of the brain. A sleep study followed by a multiple sleep latency test (MSLT), where the patient is kept at the sleep lab and allowed to take four to five naps to determine the onset of the sleep and if REM sleep occurs during any of these naps. MSLT is used to diagnose primary hypersomnia and narcolepsy.
The treatment of hypersomnia depends on the cause and the type of hypersomnia. If it is primary, or if the patient continues to experience excessive daytime sleepiness then medications can be used including Nuvigil (Armodafinil) and Provigil (modafinil). Alternative medications include stimulants (Adderall, Ritalin and others). If it is secondary hypersomnia, then treating the cause is required and should resolve it.
Narcolepsy with or without Cataplexy
Narcolepsy is a chronic neurologic disorder with abnormality in regulating the wake-sleep cycle with patients falling asleep inappropriately during the day. Cataplexy is defined as the sudden and transient loss of muscle tone, often triggered by excessive emotions such as laughing, crying, and terror that exists in 70% of patients with narcolepsy. Narcolepsy is typically the result of a genetic predisposition and abnormality in the neurotransmitter Orexin function and sensitivity. Patients with narcolepsy present with excessive daytime sleepiness and falling asleep inappropriately while in the middle of a conversation or behind the wheel, and/or watching TV, hypnagogic hallucinations, and sleep paralysis. If cataplexy is present, then the patient looses muscle tone and collapses without loss of consciousness.
Narcolepsy diagnosis begins with clinical presentation and confirmed with a multiple sleep latency test where two or more REM onsets naps are documented. Other diagnostic tools include genetic testing or a lumbar puncture to look for markers in the cerebral spinal fluid.
The treatment of narcolepsy includes Nuvigil (Armodafinil) and Provigil (modafinil). Alternative medications include stimulants (Adderall and Ritalin and others). Cataplexy on the other hand is treated with certain antidepressants such as imipramine, clomipramine, protriptyline venlafaxine, fluoxetine, paroxetine, sertraline, or citalopram. Another medication that is commonly used to treat cataplexy if the above options fail is sodium oxybate (Xyrem); which is highly regulated due to the side effect profile.
REM sleep behavior disorder (RBD):
RBD is characterized by loss of normal voluntary muscle tone during REM sleep associated with complex motor behavior while dreaming. Patients are naturally paralyzed during REM sleep to avoid acting out their dreams. In this disorder, patients are not paralyzed and they act out their dreams. This disorder can be very detrimental to the family where patients injure themselves and/or family members while asleep. RBD disorder can be primary where there is no cause can be identified or secondary where it can be related to other neurologic or metabolic disorders such as vascular lesions, brain stem cancer, demyelinating disease and MS, or autoimmune disorders.
The diagnosis of RBD is typically based on the clinical history. However, an attended overnight sleep study can aid in the diagnosis documenting the movements on video and increase muscle tone during REM sleep. At times, imaging of the brain and metabolic workup might be necessary in ruling out secondary causes.
The treatment typically starts with patient and family education about safety during the night. Medications used include clonazepam, melatonin, or Pramipexole.
Obstructive Sleep Apnea (OSA)
OSA is the most common sleep disorder where there is an increase in upper airway resistance causing the upper airways to collapse while the patient is asleep. Symptoms including snoring, breathing pauses, waking up at night with chocking sensation, waking up in the morning feeling unrefreshed, excessive sleepiness, dry mouth, morning headaches and fatigue during the day. During normal sleep, people fall into four stages of sleep (stages N1, N2, N3, and REM); Stages N3 and REM are the deep sleep where we believe the body restores itself from damages occurred during the day. In OSA patients, the upper airways collapse, the patient stops airing the lungs, oxygen saturation drops, the brain kicks the patient out of deep sleep forcing the patient to breath. When this happens several times a night, the patient ends up with fragmented and non-restorative sleep. This in turn results into the patient feeling unrefreshed in the AM, excessively sleepy and fatigued during the day. In addition, the long-term affect of this results into increasing the risk for hypertension, pulmonary hypertension, diabetes, cardiac arrhythmias, stroke, diabetes, early dementia and sudden death.
The diagnosis of OSA is based on in the initial screen of clinical symptoms and confirmed with an overnight attended sleep study in a certified sleep laboratory. During sleep study, several parameters are monitored including breathing, oxygenation, brain wave activity, and leg, abdominal and chest movements.
The first line of treatment of the OSA is CPAP, which is a machine that pushes air into the airway forcing it to stay open and preventing it from collapsing. If the patient is unable to tolerate CPAP, alternative options include oral appliances that are designed and fitted by a sleep disorder dentist or an ENT specialist, or surgery where there are multiple surgical procedures can help correct the problem. Preventative measures for sleep apnea include weight loss and maintaining ideal body weight, avoidance of sedatives and hypnotics that might worsen the symptoms.
OSA if left untreated in has immediate affects and long term complications. Immediate effects are snoring, dry mouth, feeling unrefreshed when waking up in the morning, morning headaches, excessive daytime sleepiness, depression, anxiety. Long term complications include hypertension, pulmonary hypertension, diabetes, heart attacks, cardiac arrhythmias, dementia and sudden death.
Restless Leg Syndrome (RLS)
RLS is a neurological disorder characterized by an irresistible urge to move one’s limbs to stop uncomfortable or odd sensations. It most commonly affects the legs, but can affect the arms, torso, and even phantom limbs. Although symptoms are more common at night but they can occur during the day especially during inactivity. RLS can be associated with other disorders including iron deficiency, diabetes, lower back pain, rheumatoid arthritis, B12 deficiency, frequent blood donation, antidepressant medications, alcohol, and caffeine.
The diagnosis of RLS is based on criteria including compelling urges to move the legs, occurring at rest, and improves with activity and walking. Periodic limb movement disorder (PLMD) is associated with RLS, typically diagnosed with a sleep study.
The approach to treating the RLS includes correcting the metabolic abnormality such as iron deficiency, thyroid disease, diabetes and others then treat with medications. The pharmacological treatment includes dopamine agonist (Requip, Mirapex), carbidoba/levodopa (Sinemet), anticonvulsants (gabapentin), opioids (hydrocodone, oxycodone.). If PLMD is also present with RLS, clonazepam should be considered first.
Shift Work Disorder (SWD)
SWD is defined as sleep disturbances due to working at night or rotating shifts between night and day. It involves a problem with the 24-hour internal clock (circadian rhythm) regulating the light and dark circle for the individual. It is usually seen in people who work night shifts.
The diagnosis is based on the history obtain from the patient and at times the patient is given a sleep diary to write down sleep and wake times. It is essential to diagnose and treat this disorder since it is associated with increase risks of infections, breast and prostate cancer, high cholesterol, heart attacks, and obesity.
The treatment for this disorder can be difficult since the ultimate treatment is to switch to a regular work schedule, which will improve the sleep hygiene and sleep cycle and therefore eliminate the problem. Other modalities that can be helpful are controlling the light, sound, and temperature. Light therapy can be used and the patient’s education and counseling is helpful. At times pharmacotherapy can be used including Ambien, Sonata, Lunesta, Rozerem and at times the stimulants such as modafinil and Armodafinil can be used during the wakefulness to maintain wakefulness.