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Prepared by navjot brar and kawaljit kang, MSc 2nd yr, Mai Bhago College of Nursing, Tarn-Taran

Bulbar palsy
Bulbar palsy refers to impairment of function of the cranial nerves IX, X, XI and XII, which occurs due to a lower motor neuron lesion either at nuclear or fascicular level in the medulla oblongata or from lesions of the lower cranial nerves outside the brainstem In contrast, pseudobulbar palsy describes impairment of function of cranial nerves IX-XII due to upper motor neuron lesions of the corticobulbar tracts in the mid-pons. For clinically evident dysfunction to occur, such lesions must be bilateral as these cranial nerve nuclei receive bilateral innervation. Causes Genetic: Kennedy's disease is a debilitating neurodegenerative disease resulting in muscle cramps and progressive weakness due to degeneration of motor neurons in the brain stem and spinal cord. acute intermittent porphyria is a rare autosomal dominant[1] metabolic disorder affecting the production of heme, the oxygen-binding prosthetic group of hemoglobin. It is characterized by a deficiency of the enzyme porphobilinogen deaminase. Vascular causes: medullary infarction Degenerative diseases: motor neuron disease (amyotrophic lateral sclerosis), syringobulbia is a medical condition when syrinxes, or fluid filled cavities, affect the brainstem. This defect normally results from congenital abnormality, trauma or tumor growth. Inflammatory/infective: Guillain-Barr syndrome, poliomyelitis, Lyme disease Malignancy: brain-stem glioma Toxic: botulism Autoimmune: myasthenia gravis Symptoms dysphagia (difficulty in swallowing) difficulty in chewing nasal regurgitation slurring of speech choking on liquids Dysphonia (defective use of the voice)

Prepared by navjot brar and kawaljit kang, MSc 2nd yr, Mai Bhago College of Nursing, Tarn-Taran

Dysarthria (difficulty in articulating words due a CNS problem) Dysphasia (difficulty in using or understanding words due to injury or disease of the brain) Signs Nasal speech lacking in modulation and difficulty with all consonants Tongue is atrophic and shows fasciculations. Dribbling of saliva. Weakness of the soft palate, examined by asking the patient to say aah. The jaw jerk is normal or absent. The gag reflex is absent. In addition, there may be lower motor neuron lesions of the limbs.

The occular muscles are spared and this differentiates it from myasthenia gravis. Pseudobulbar palsy is a clinical syndrome similar to bulbar palsy but the damage is occurred in upper motor neurons, that is the nerves cells come down from the cerebral cortex inervating the motor nuclei in the medulla. This is usually caused by stroke. Bulbar Palsy Diagnosis With bulbar palsy, the diagnostic tests to be done would be the same as the tests done in amyotrophic lateral disease. firstly, a thorough physical examination neurologic functions. A family history as well as patients history will also be collected. Routine blood test and urine samples MRI or magnetic resonance imaging electromyography is a test wherein it records the muscle activity of the patients body nerve conduction tests, it examines how fast do nerve cells transmit impulses.

Bulbar Palsy Treatment As of the present, there is still no precise treatment for the problem. most physicians and the health care team would assist in making the patients life easier. Since body weakness is generally noted, a caregiver should always be present to help the patient move around, feed him or her and ensure that choking will not happen. having a physical therapy is essential to maintain the strength thats left off the client and avoid shortening of the muscles. A speech therapist may also be hired to help the patient speak clearly.

Prepared by navjot brar and kawaljit kang, MSc 2nd yr, Mai Bhago College of Nursing, Tarn-Taran

There are some drugs prescibred by the doctor like Baclofen and phenytoin to avoid muscle spasm and decrease the likelihood of cramps. Since the patient may also be charged emotionally, anti-depressants may also be given to the patient. Bulbar Palsy Prognosis Experts conclude that the prognosis for this problem is fairly poor. The exact cure for the problem is still unknown and the treatment is focused on the giving support and minimizing the aggressive degeneration of neurons rather than completely reversing the damage. The lifespan of most patients after having been diagnosed with the disease is from 1 to 3 years

Arteriovenous fistula
An arteriovenous fistula is an abnormal connection or passageway between an artery and a vein. It may be congenital, surgically created forhemodialysis treatments, or acquired due to pathologic process, such as trauma or erosion of an arterial aneurysm. Causes

Congenital (developmental defect) Rupture of arterial aneurysm in adjacent vein Penetrating injuries Inflammatory necrosis of adjacent vessels Intentionally created (for example, Cimino hemodialysis)

fistula as

vascular

access

for

Pathophysiology When an arteriovenous fistula is formed involving a major artery like the abdominal aorta, it can lead to a large decrease in peripheral resistance. This lowered peripheral resistance causes the heart to increase cardiac output to maintain proper blood flow to all tissues. The physical manifestations of this would be a relatively normal systolic blood pressure with a decreased diastolic blood pressure resulting in a wide pulse pressure. Normal blood flow in the brachial artery is 85 to 110 milliliters per minute (mL/min). After the creation of a fistula, the blood flow increases to 400500 mL/min immediately, and 7001,000 mL/min within 1 month. A bracheocephalic fistula above the elbow has a greater flow rate than a radiocephalic fistula at the wrist. Both the artery and the vein dilate and elongate in response to the greater blood flow and shear stress, but the vein dilates more and becomes "arterialized". In one study, the cephalic vein increased from 2.3 mm to 6.3 mm diameter after 2 months. When the vein is large enough to allow cannulation, the fistula is defined as "mature." An arteriovenous fistula can increase preload.
Prepared by navjot brar and kawaljit kang, MSc 2nd yr, Mai Bhago College of Nursing, Tarn-Taran

Complications Just like berry aneurysm, an causing subarachnoid hemorrhage. intracerebral arteriovenous fistula can rupture

Carotid-cavernous fistula
A carotid-cavernous fistula (CCF) results from an abnormal communication between the arterial and venous systems within the cavernous sinus in the skull. It is a type of arteriovenous fistula. As arterial blood under high pressure enters the cavernous sinus, the normal venous return to the cavernous sinus is impeded and this causes engorgement of the draining veins, manifesting most dramatically as a sudden engorgement and redness of the eye of the same side. Causes Carotid cavernous fistulae may form following closed or penetrating head trauma, surgical damage, rupture of an intracavernous aneurysm, or in association with connective tissue disorders, vascular diseases and dural fistulas. Classification low-flow or high-flow traumatic or spontaneous direct or indirect The traumatic CCF typically occurs after a basal skull fracture. The spontaneous dural cavernous fistula which is more common usually results from a degenerative process in older patients with systemic hypertension and atherosclerosis. Direct fistulas occur when the Internal Carotid artery (ICA) itself fistulizes into the Cavernous sinus whereas indirect is when a branch of the ICA or External Carotid artery (ECA) communicates with the cavernous sinus. A popular classification divides CCF into four varieties depending on the type of arterial supply. Type Description

Fistulous supply from the internal carotid artery

Supply from the dural branches of internal carotid artery

Prepared by navjot brar and kawaljit kang, MSc 2nd yr, Mai Bhago College of Nursing, Tarn-Taran

Supply from the dural branches of external carotid artery

Combined forms

Presentation

dilated blood vessels in the eye in CCF [1] CCF symptoms include bruit (a humming sound within the skull due to high blood flow through the arteriovenous fistula), progressive visual loss, and pulsatileproptosis or progressive bulging of the eye due to dilatation of the veins draining the eye. Pain is the symptoms that patients often find the most difficult to tolerate. Patients usually present with sudden or insidious onset of redness in one eye, associated with progressive proptosis or bulging. They may have a history of similar episodes in the past. Diagnosis

Selective angiography of the external carotid artery showing an indirect type D right carotid cavernous fistula, filling of the cavernous sinus (arrow) and retrograde drainage into the right superior ophthalmic vein (arrowhead) MRI scan, magnetic resonance angiography CT scan A cerebral digital subtraction angiography (DSA) enhances visualization of the fisula.
Prepared by navjot brar and kawaljit kang, MSc 2nd yr, Mai Bhago College of Nursing, Tarn-Taran

CT scans show diffuse enlargement of all the extraocular muscles resulting from venous engorgement and a characteristically enlarged superior ophthalmic vein. Selective arteriography is used to evaluate arteriovenous fistulas.

Treatment The mainstay of treatment for CCF is endovascular therapy. This may be transarterial (mostly in the case of direct CCF) or transvenous (most commonly in indirect CCF). Occasionally, more direct approaches, such as direct transorbital puncture of the cavernous sinus or cannulation of the draining superior orbital vein are used when conventional approaches are not possible. Spontaneous resolution of indirect fistulae has been reported but is uncommon. Staged manual compression of the ipsilateral carotid has been reported to assist with spontaneous closure in selected cases. Direct CCF may be treated by occlusion of the affected cavernous sinus (coils, balloon, liquid agents), or by reconstruction of the damaged internal carotid artery (stent, coils or liquid agents). Indirect CCF may be treated by occlusion of the affected cavernous sinus with coils, liquid agents or a combination of both.

Bell's palsy
Bell's palsy is a disorder of the nerve that controls movement of the muscles in the face. This nerve is called the facial or 7th cranial nerve. Damage to this nerve causes weakness or paralysis of these muscles. Paralysis means that you cannot use the muscles at all. Bell's palsy is a form of facial paralysis resulting from a dysfunction of the cranial nerve VII (the facial nerve) that results in the inability to control facial muscles on the affected side. Several conditions can cause facial paralysis, e.g., brain tumor, stroke, and Lyme disease. However, if no specific cause can be identified, the condition is known as Bell's palsy. Named after Scottish anatomist Charles Bell, who first described it, Bell's palsy is the most common acute mononeuropathy (disease involving only one nerve) and is the most common cause of acute facial nerve paralysis. Bell's palsy is defined as an idiopathic unilateral facial nerve paralysis, usually self-limiting. The hallmark of this condition is a rapid onset of partial or complete paralysis that often occurs overnight. In rare cases (<1%), it can occur bilaterally resulting in total facial paralysis. It is thought that an inflammatory condition leads to swelling of the facial nerve. The nerve travels through the skull in a narrow bone canal beneath the ear. Nerve swelling and compression in the narrow bone canal are thought to lead to nerve inhibition, damage or death. No readily identifiable cause for Bell's palsy has been found.
Prepared by navjot brar and kawaljit kang, MSc 2nd yr, Mai Bhago College of Nursing, Tarn-Taran

Causes, incidence, and risk factors

Bell's palsy affects about 30,000 - 40,000 people a year in the United States. Bell's palsy involves damage to the seventh cranial (facial) nerve. This nerve controls the movement of the muscles of the face. Bell's palsy is thought to be due to swelling (inflammation) of this nerve in the area where it travels through the bones of the skull. The cause is often not clear. A type of herpes infection called herpes zoster might be involved. Other conditions that may cause Bell's palsy include:

HIV infection Lyme disease Middle ear infection Sarcoidosis

Symptoms Sometimes you may have a cold shortly before the symptoms of Bell's palsy begin. Symptoms most often start suddenly, but may take 2 - 3 days to show up. They do not become more severe after that. Symptoms are almost always on one side of the face only. They may range from mild to severe. The face will feel stiff or pulled to one side, and may look different. Other symptoms can include:

Difficulty closing one eye Difficulty eating and drinking; food falls out of one side of the mouth Drooling due to lack of control over the muscles of the face Drooping of the face, such as the eyelid or corner of the mouth Problems smiling, grimacing, or making facial expressions Twitching or weakness of the muscles in the face

Other symptoms that may occur: Dry eye, which may lead to eye sores or infections Dry mouth Headache Loss of sense of taste Sound that is louder in one ear (hyperacusis) Twitching in face

The facial nerves control a number of functions, such as blinking and closing the eyes, smiling, frowning, lacrimation, salivation, flaring nostrils and raising eyebrows. They also innervate the stapedial (stapes) muscles of the middle ear and carry taste sensations from the anterior two-thirds of the tongue.
Prepared by navjot brar and kawaljit kang, MSc 2nd yr, Mai Bhago College of Nursing, Tarn-Taran

Clinicians should determine whether the forehead muscles are spared. Due to an anatomical peculiarity, forehead muscles receive innervation from both sides of the brain. The forehead can therefore still be wrinkled by a patient whose facial palsy is caused by a problem in one of the hemispheres of the brain (central facial palsy). If the problem resides in the facial nerve itself (peripheral palsy) all nerve signals are lost on the ipsilateral (same side of the lesion) half side of the face, including to the forehead (contralateral forehead still wrinkles). The degree of nerve damage can be assessed using the House-Brackmann score. Because both the nerve to Stapedius and the chorda tympani nerve (taste) are branches of the facial nerve, patients with Bell's palsy may present withhyperacusis or loss of taste sensation in the anterior 2/3 of the tongue. Signs and tests Often, Bell's palsy can be diagnosed just by taking a health history and doing a complete physical exam. If your health care provider is worried that a brain tumor is causing your symptoms, you may need: CT scan of the head Magnetic resonance imaging (MRI) of the head Sometimes, you will need a test to check the nerves that supply the muscles of your face:

Electromyography (EMG) Nerve conduction test

Treatment Often, no treatment is needed. Symptoms often begin to improve right away. However, it may take weeks or even months for the muscles to get stronger, and this may be frustrating. Your health care provider may give you lubricating eye drops or eye ointments to keep the surface of the eye moist if you cannot close it completely. You may need to wear an eye patch while you sleep. Sometimes medicines may be used, but it is not clear how much they help. If medicines are used, they should be started right away.

Corticosteroids may reduce swelling around the facial nerve Medications can fight the virus that may be causing Bell's palsy

Surgery to relieve pressure on the nerve (decompression surgery) has not been shown to benefit most people with Bell's palsy. Bell's palsy affects each individual differently. Steroids have been shown to be effective at improving recovery while antivirals have not. Steroids
Prepared by navjot brar and kawaljit kang, MSc 2nd yr, Mai Bhago College of Nursing, Tarn-Taran

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Corticosteroid such as prednisone significantly improves recovery at 6 months and are thus recommended. Early treatment (within 3 days after the onset) is necessary for benefit with a 14% greater probability of recovery. Antivirals Antivirals (such as acyclovir) are ineffective in improving recovery from Bell's palsy beyond steroids alone. They were however commonly prescribed due to a theoretical link between Bell's palsy and the herpes simplex and varicella zoster virus. Physiotherapy Physiotherapy can be beneficial to some individuals with Bells palsy as it helps to maintain muscle tone of the affected facial muscles and stimulate the facial nerve. It is important that muscle re-education exercises and soft tissue techniques be implemented prior to recovery in order to help prevent permanent contractures of the paralyzed facial muscles. To reduce pain, heat can be applied to the affected side of the face. Surgery Surgery may be able to improve outcomes in facial nerve palsy that has not recovered. A number of different techniques exist. Smile surgery or smile reconstruction is a surgical procedure that may restore the smile for people with facial nerve paralysis. It is unknown if early surgery is beneficial or harmful. Adverse effects include hearing loss which occurs in 315% of people. As of 2007 the American Academy of Neurology did not recommend surgical decompression. Complementary therapy The efficacy of acupuncture remains unknown because the available studies are of low quality (poor primary study design or inadequate reporting practices). prognosis Most cases go away completely within a few weeks to months. If you did not lose all of your nerve function and symptoms began to improve within 3 weeks, you're more likely to regain all or most of the strength in your facial muscles. Sometimes, the following symptoms still may be present:

Long-term changes in taste Spasms of muscles or eyelids Weakness that remains in facial muscles
Prepared by navjot brar and kawaljit kang, MSc 2nd yr, Mai Bhago College of Nursing, Tarn-Taran

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Complications Excess drying of the eye surface, leading to eye sores or infections. Corticosteroids have been found to improve outcomes, when used early, while anti-viral drugs have not. Most people recover spontaneously and achieve near-normal to normal functions. Many show signs of improvement as early as 10 days after the onset, even without treatment. Often the eye in the affected side cannot be closed. The eye must be protected from drying up, or the cornea may be permanently damaged resulting in impaired vision. In some cases denture wearers experience some discomfort.

Trigeminal neuralgia
(Tic douloureux)
Trigeminal neuralgia is a nerve disorder that causes a stabbing or electric-shock-like pain in parts of the face. Trigeminal neuralgia (TN, or TGN), also known as prosopalgia,]suicide
disease, or Fothergill's disease is a neuropathic disorder characterized by episodes of intense pain in

the face, originating from the trigeminal nerve.

Causes, incidence, and risk factors The pain of trigeminal neuralgia comes from the trigeminal nerve. This nerve carries the feelings of touch and pain from the face, eyes, sinuses, and mouth to the brain. The condition usually affects adults, but it may affect anyone at any age. Trigeminal neuralgia may be part of the normal aging process. Trigeminal neuralgia may be caused by:

Multiple sclerosis Pressure on the trigeminal nerve from a swollen blood vessel or tumor

Often, no cause is found. Doctors are more likely to find a cause in a person who is younger than age 40.
Prepared by navjot brar and kawaljit kang, MSc 2nd yr, Mai Bhago College of Nursing, Tarn-Taran

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Symptoms Very painful, sharp electric-like spasms that usually last a few seconds or minutes, but can become constant Pain is usually only on one side of the face, often around the eye, cheek, and lower part of the face Pain may be triggered by touch or sounds Painful attacks of trigeminal neuralgia can be triggered by common, everyday activities, such as: o Brushing teeth o Chewing o Drinking o Eating o Lightly touching the face o Shaving Signs and tests A brain and nervous system (neurologic) examination is usually normal. Tests that are done to look for the cause of the problem include:

Blood tests MRI of the head Trigeminal reflex testing

Treatment Your primary care physician, a neurologist, or a pain specialist may be involved in your care. Certain medicines sometimes help reduce pain and the rate of attacks. These medicines include:

Anti-seizure drugs (carbamazepine, gabapentin, lamotrigine, phenytoin, valproate, and pregabalin) Muscle relaxants (baclofen, clonazepam)

Tricyclic antidepressants (amitriptyline, nortriptyline, or carbamazepine)

Some patients may need surgery to relieve pressure on the nerve. Techniques include:
Prepared by navjot brar and kawaljit kang, MSc 2nd yr, Mai Bhago College of Nursing, Tarn-Taran

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Cutting or destroying part of the trigeminal nerve Destroying the trigeminal nerve with a needle or probe placed through the skin using radiofrequency ablation or an injection of glycerol Electrostimulation Percutaneous balloon microcompression Removal of the tumor (when a tumor is the cause) Stereotactic radiosurgery (Gamma knife) Surgery to remove a blood vessel that is putting pressure on the trigeminal nerve (called microvascular decompression, or MVD)

Management As with many conditions without clear physical or laboratory diagnosis, TN is sometimes misdiagnosed. A TN sufferer will sometimes seek the help of numerous clinicians before a firm diagnosis is made. There is evidence that points towards the need to quickly treat and diagnose TN. It is thought that the longer a patient suffers from TN, the harder it may be to reverse the neural pathways associated with the pain. The dentist must ensure a correct diagnosis does not mistake TN as a temporomandibular disorder. Since triggering may be caused by movements of the tongue or facial muscles, TN must be differentiated from masticatory pain that has the clinical characteristics of deep somatic rather than neuropathic pain. Masticatory pain will not be arrested by a conventional mandibular local anesthetic block. Dentists who suspect TN should proceed in the most conservative manner possible and should ensure that all tooth structures are "truly" compromised before performing extractions or other procedures. Medical

The anticonvulsant carbamazepine is the first line treatment; second line medications include baclofen, lamotrigine, oxcarbazepine, phenytoin, gabapentin, and sodium valproate. Uncontrolled trials have suggested that clonazepam and lidocaine may be effective. Low doses of some antidepressants such as amitriptyline are thought to be effective in treating neuropathic pain, but a tremendous amount of controversy exists on this topic, and their use is often limited to treating the depression that is associated with chronic pain, rather than the actual sensation of pain from the trigeminal nerve. Antidepressants are also used to counteract a medication side effect.

Prepared by navjot brar and kawaljit kang, MSc 2nd yr, Mai Bhago College of Nursing, Tarn-Taran

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Duloxetine can also be used in some cases of neuropathic pain, and as it is also an antidepressant can be particularly helpful where neuropathic pain and depression are combined. Opiates such as morphine and oxycodone can be prescribed, and there is evidence of their effectiveness on neuropathic pain, especially if combined with gabapentin.

Surgical The evidence for surgical therapy is poor and it is thus only recommended if medical treatment is not effective. While there may be pain relief there is also frequently numbness post procedure. Microvascular decompression appears to result in the longest pain relief. Percutaneous radiofrequency thermorhizotomy may also be effective as may gamma kniferadiosurgery, however the effectiveness decreases with time. Three other procedures use needles or catheters that enter through the face into the opening where the nerve first splits into its three divisions. Some excellent success rates using a costeffectivepercutaneous surgical procedure known as balloon compression have been reported. This technique has been helpful in treating the elderly for whom surgery may not be an option due to coexisting health conditions. Balloon compression is also the best choice for patients who have ophthalmic nerve pain or have experienced recurrent pain after microvascular decompression. Glycerol injections involve injecting an alcohol-like substance into the cavern that bathes the nerve near its junction. This liquid is corrosive to the nerve fibers and can mildly injure the nerve enough to hinder the errant pain signals. In a radiofrequency rhizotomy, the surgeon uses an electrode to heat the selected division or divisions of the nerve. Done well, this procedure can target the exact regions of the errant pain triggers and disable them with minimal numbness. prognosis How well you do depends on the cause of the problem. If there is no disease causing the problem, treatment can provide at least some relief. However, the pain may become constant and severe in some patients.

Prepared by navjot brar and kawaljit kang, MSc 2nd yr, Mai Bhago College of Nursing, Tarn-Taran