How to treat Acute Bacterial Infection?

Clinical Features and Treatment of Bacterial Infection:

imagesIn most cases the infection causing meningitis arises in the nasopharynx intravascular invasion (bacteraemia) and penetration of the blood brain barrier follow mucosal involvement with entry into the CSF. Bacteria may invade the subarachnoid space directly by spread from contiguous structures, e.g. sinuses and fractures. Specific characteristics of the capsule determine whether meninges are breached. Humoral defences against bacteria are absent in the CSF offering little resistance to infection.

Clinical Features

The classical clinical traid is

Prodromal Features

A respiratory infection otitis media or pneumonia associated with muscle pain.

Meningitic Symptoms

  • Severe frontal/occipital headache
  • Stiff neck
  • Photophobia

Investigations

  • If patient has altered consciousness, focal signs, papilloedema, and a recent seizure or is immunocompromised a CT brain should be done before LP. However, do not delay treatment -take blood cultures and commence antibiotics prior to scanning.
  • If above signs are absent or CT scan excludes a mass lesion confirm diagnosis with a lumbar puncture and identify the organism.

Treatment

  • Once meningitis is suspected, treatment must commence immediately, often before identification of the causative organism.
  • Antibiotics must penetrate CSF, be in appropriate bactericidal dosage and be sensitive to causal organism once identified.

Braner Pain Clinics specialize in chronic pain management, neurology, neurological testing and disability. Our clinics are conveniently located in Northern Virginia minutes away from Interstate 495 (Beltway). Call now for best treatment: (703) 573-1282

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How to prevent Anterior Cerebral Artery (Stroke)?

Clinical Features of Anterior Cerebral Artery:

imagesThe anterior cerebral artery is a branch of the internal carotid and runs above the optic nerve to follow the curve of the corpus callosum. Soon after its origin the vessel is joined by the anterior communicating artery. Deep branches pass to the anterior part of the internal capsule and basal nuclei. Cortical branches supply the medial surface of the hemisphere:

Clinical Features

The anterior cerebral artery may be occluded by embolus or thrombus. The clinical picture depends on the site of occlusion (especially in relation to the anterior communicating artery) and anatomical variation, e.g. both anterior cerebral arteries may arise from one side by enlargement of the anterior communicating artery.

Occlusion proximal to the anterior communicating artery is normally well tolerated because of the cross flow.

  • Distal occlusion results in weakness and cortical sensory loss in the contralateral lower limb with associated incontinence. Occasionally a contralateral grasp reflex is present.
  • Proximal occlusion when both anterior cerebral vessels arise from the same side results in ‘cerebral’ paraplegia with lower limb weakness, sensory loss, incontinence and presence of grasp, snout and palmomental reflexes.

Bilateral frontal lobe infarction may result in akinetic mutism or deterioration in conscious level.

Braner Pain Clinics has a talented and friendly staff. We will do everything in our power to make sure your visit is a satisfying experience. If there is anything else you may need from us, just ask! We are here to serve you. Contact Us at: (877) 573-1282 or Visit Our Website: http://www.branerpainclinic.com

Can Cerebral Aneurysms be prevented?

Risk Factors and Complications of Cerebral Aneurysms (Brain Injury):

indexA Cerebral Aneurysm is a huge, weak area in the wall of an artery that supplies blood vessels to the mind. In most situations, a brain aneurysm causes no symptoms and goes unseen. In rare situations, the brain aneurysm bursts, launching blood vessels into the head and causing a heart stroke.

Risk Factors

Pathogenesis

The cause of aneurysm formation may be multifactorial with acquired factors combining with an underlying genetic susceptibility.

  • Aneurysms were once thought to be ‘congenital’ due to the finding of developmental defects in the tunica media.
  • Aneurysms often form at sites of haemodynamic stress where for example, a congenitally hypoplastic vessel leads to excessive flow in an adjacent artery.
  • It is not known whether they form rapidly over the space of a few minutes, or more slowly over days, weeks, or months.

Clinical Presentation

Of those patients with intracranial aneurysms presenting acutely, most have had a subarachnoid haemorrhage. A few present with symptoms or signs due to compression of adjacent structures. Others present with an aneurysm found incidentally.

1. Rupture

The features of SAH have already been described in detail; they include sudden onset of headache, vomiting, neck stiffness, loss of consciousness, focal signs and epilepsy. Since the severity of the haemorrhage relates to the patients clinical state and this in turn relates to outcome, much emphasis has been placed on categorising patients into 5 level grading systems, e.g. Hunt and Hess.

2. Compression from Aneurysm

A large internal carotid artery aneurysm (or anterior communicating artery aneurysm) may compress.

3. Incidental Finding

The improved availability of sensitive high quality, non-invasive MR or CT imaging techniques has greatly increased the number of patients in whom an intracranial aneurysm is detected incidentally, during investigation for other disease.

Complications of Aneurysmal

INTRACRANIAL

  • Rebleeding
  • Cerebral ischaemia/infarction
  • Hydrocephalus
  • ‘Expanding’ haematoma
  • Epilepsy

EXTRACRANIAL

  • Myocardial infarction
  • Cardiac arrhythmias
  • Pulmonary oedema
  • Gastric haemorrhage (stress ulcer)

Braner Clinics is a professional corporation, and was established for the practice of chronic pain management in 1990. Pain Management is the specialty of Pain Medicine for the assessment, diagnosis and care of severe, chronic persistent pain conditions. Call Now for Quick Appointment: 1 (877) 573-1282

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How to cure Chronic Subdural Haematoma (Head Injury)?

Clinical Features and Diagnosis of Subdural Haematoma (Head Injury):

imagesSubdivision of subdural haematomas into acute and subacute forms serves no practical purpose. Chronic subdural haematoma however is best considered as a separate entity, differing both in presentation and management.

  • Chronic subdural haematomas – fluid may range from a faint yellow to a dark brown colour.
  • A membrane grows out from the dura to envelop the haematoma.
  • Chronic subdural haematomas occur predominantly in infancy and in the elderly. Trauma is the likely cause, although a history of this is not always obtained.

Predisposing factors

Breakdown of protein within the haematoma and a subsequent rise in osmotic pressure was originally believed to account for the gradual enlargement of the untreated subdural haematoma. Studies showing equality of osmotic pressures in blood and haematoma fluid cast doubt on this theory and recurrent bleeding into the cavity is now known to play an important role.

Clinical Features

  • Dementia.
  • Deterioration in conscious level, occasionally with fluctuating course.
  • Symptoms and signs of raised ICP.
  • Focal signs occasionally occur, especially limb weakness. This may be ipsilateral to the side of the lesion, i.e. a false localising sign.

Diagnosis

  • CT Scan appearances depend on the time between the injury and the scan.
  • With injuries 1-3 weeks old, the subdural haematoma may be isodense with brain tissue. In this instance, i.v. contrast enhancement may delineate the cortical margin.
  • Beyond 3 weeks subdural haematomas appear as a low density lesion.

Adult

  • The haematoma is evacuated through two or three burr holes and the cavity is irrigated with saline. Drains may be left in the subdural space and nursing in the head-down position may help prevent recollection.
  • Craniotomy with excision of the membrane is seldom required.
  • In patients who have no depressed conscious level, conservative treatment with steroids over several weeks may result in resolution.

Infants

The haematoma is evacuated by repeated needle aspiration through the anterior fontanelle. Persistent subdural collections require a subdural peritoneal shunt. As in adults, craniotomy is seldom necessary.

Braner Pain Clinics specialize in chronic pain management, neurology, neurological testing and disability. Our clinics are conveniently located in Northern Virginia minutes away from Interstate 495 (Beltway). Call today at: (703) 573-1282

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How to prevent Brachial Plexus Injury?

Symptoms and Treatment of Brachial Plexus:

The Brachial Plexus lies in the posterior triangle of the neck between the muscles scalenius anterior and scalenius medius. At the root of the neck the plexus lies behind the clavicle. The plexus itself gives off several important branches:

In this rare disorder the brachial plexus, subclavian artery and subclavian vein may be compressed in the neck by contiguous structures such as a cervical rib or tight fibrous band.

Brachial Plexus

Symptoms

Pain in the neck and shoulder with paraesthesia in the forearm, made worse by carrying a suitcase, shopping bag, etc.

Signs

1.   Sensory loss in a T1 distribution.

2.   Wasting and weakness of thenar and occasionally interosseous muscles.

3.   Signs of vascular compression:

  • Unilateral Raynaud’s phenomenon.
  • Pallor of limb on elevation.
  • Brittle trophic finger nails.
  • Loss of radial pulse in arm on abduction and external rotation at the shoulder or on bracing the shoulders.
  • Subclavian venous thrombosis may occur, especially after excessive usage of arm.

Investigation

  • Coronal MRI is the definitive investigation.
  • Plain radiology of the thoracic outlet may reveal a cervical rib or prolonged transverse process.
  • Nerve conduction/electromyography will distinguish this from other peripheral nerve lesions.
  • Arteriography or venography is occasionally necessary if there are obvious vascular problems.

Treatment

  • In middle-aged people with poor posture and no evidence of abnormality on plain radiology, neck and postural exercises are helpful.
  • In younger patients with clinical and electrophysiological changes supporting the radiological abnormalities, exploration and removal of a fibrous band or rib may afford relief.

Brachial plexus injuries are common in sport activities, but they frequently result from auto or slip and fall injuries or drops. Braner Pain Clinics specialize in chronic pain management, neurology, neurological testing and disability. Call now for best treatment: 1 (877) 573-1282

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How do you treat patients with Muscle Pain (Myalgia)?

Investigations And Types of Myalgia:Muscle Pain (Myalgia)

Muscle pain is a common medical complaint. There are many causes and clinical evaluation and appropriate investigation is often difficult. The physiological mechanisms producing such a symptom are limited.

  • Mechanical Pain: results from excessive muscle tension or contraction and is cramp like.
  • Inflammatory Pain: results from disruption of muscle fibres, inflammatory exudates and fibre swelling.
  • Ischaemic Pain: results from metabolic change, usually in response to exercise and is deep and aching.

Muscle pain may be physiological – as a consequence of extreme exercise or pathological – as a consequence of muscle, soft tissue or systemic illness.

DIAGNOSTIC APPROACH TO MUSCLE PAIN

History:

Is muscle pain

Present at rest

Present with exercise

  • Physiological
  • Metabolic myopathies
  • Benign myalgic encephalomyelitis  (ME)

Localized

Generalized

  • Polymyalgia rheumatica
  • Parkinson’s disease
  • Metabolic myopathies
  • Inflammatory myopathies
  • Benign myalgic encephalomyelitis (ME)

Family History

Exposure to toxins

  • Drug induced myopathies
  • Alcoholic myopathy

Examination:

Is There

Wasting/Weakness

Skin Rash

  • Inflammatory myopathy (dermatomyositis)
  • Collagen vascular disease

Stiffness or Spasms

  • Tetanus
  • Tetany
  • Spasticity
  • Neuroleptic malignant syndrome
  • Malignant hyperthermia

Muscle Swelling

  • Muscle abscess, tumors
  • Metabolic myopathy

INVESTIGATIONS OF MUSCLE PAIN

1 Serum Creatine Kinase (muscle enzyme)

2. Imaging (occasionally used)

  • Ultrasound, MR or CT in suspected muscle haematoma, abscess or tumors.
  • Radionuclide (Gallium or in suspected muscle abscess, Technetium)

3. Electromyography (EMG)

  • Will confirm presence of myopathy (rarely more specific)

4. Muscle Biopsy (needle or open)

  • Inflammatory myopathies metabolic myopathies
  • Helpful in collagen vascular disease

5. Ischaemic Lactate Test

  • Measurement of post exercise changes in serum lactate
  • Reduced response in-metabolic

Following extensive investigation, in a significant number of cases no cause of myalgia is found.

TYPES OF MUSCLE PAIN:

Most disorders are covered in relevant sections. Those that are not are briefly described.

1. Fibromyalgia

A common condition of uncertain pathology in which generalized muscle pain with localized tender areas occurs without objective clinical or laboratory abnormalities. Psychiatric symptoms commonly co-exist.

2. Malignant Hyperpyrexia

Characterized by a sudden rise in body temperature whilst undergoing general anesthesia usually with halothane or succinylcholine. Certain hereditary myopathic disorders e.g. myotonic dystrophy central core disease – are unduly prone to this condition.

3. Muscle Abscess

Commonly Staphylococcal due to local trauma or blood-borne in debilitated persons.

4. Polymyalgia Rheumatica

Proximal muscle pain encountered in the elderly and often associated with giant cell arteritis. The ESR is elevated and the EMG is normal. Muscle biopsy shows type 2 fibre losses. Steroids are effective.

5. Muscle Tumors

These are rare Mixed pathological and of varying degrees of malignancy.

6. Chronic Fatigue Syndrome/Myalgic Encephalomyelitis (CFS/ME)

An idiopathic disorder that may follow viral illness is often associated with exercise induced muscle pain and associated with fatigue. No clear underlying pathology has been found and diagnosis is based on symptoms and exclusion of other pathology. May respond to graded exercise, tricyclic antidepressants or cognitive behavioral therapy.

Muscle pain is your body’s way of telling you about a problem. See your doctor if your myalgia is prolonged and persistent or if it is accompanied by other symptoms.Talk to your doctor about muscle relaxants to that may help ease your muscle pain.Call Us Immediately if you have: 1 (877) 573-1282.

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How do you get relief from Parkinson’s Disease?

Clinical Features , Diagnosis And Treatment of Parkinson’s Disease:Parkinson’s Disease

AETIOLOGY                                 

The causes of Parkinson disease are unknown. Gene mutations have been identified in young onset and familial cases (synuclein, parkin and LRRK2).

Parkinson disease in humans and animals has resulted in increased interest in the role of toxins and an animal model for developing new treatments.

Parkinsonian features may be present in many disorders and are not always treatment (L Dopa) responsive. These disorders usually share features of slowness and rigidity (kinetic rigid syndromes)

1.Parkinson’s disease                    

  • Mimics  – Multiple system atrophy (MSA)
  • Progressive supranuclear palsy (PSP)
  • Corticobasal ganglionic degeneration
  • Diffuse Lewy body disease (DLBD)

2. Secondary Parkinsonism

  • Drug induced (dopamine receptor blockers-antipsychotics/antiemetics; sodium valproate)
  • Post traumatic (pugilists encephalopathy)
  • Vascular disease (small vessel multi-infarct state)
  • Infectious (post encephalitic/prion disease/HIV)
  • Miscellaneous: hydrocephalus/parathyroid/paraneoplastic

Pathology of Idiopathic

The substantia nigra contains pigmented cells (neuromelanin) which give it a characteristic ‘black’ appearance (macroscopic). These cells are lost in Parkinson’s disease and substantia nigra becomes pale. Remaining cells contain atypical eosinophillic inclusions in the cytoplasm. Lewy bodies may be found in the cerebral cortex especially when dementia is present (diffuse Lewy body disease). Changes are seen in other basal nuclei striatum and globus pallidus.

CLINICAL FEATURES

  • Initial symptoms are vague, the patient complains of aches and pains.
  • A coarse TREMOR at a rate of 4-7 Hz usually develops early in the disease.
  • It begins unilaterally in the upper limbs and eventually spreads to all four limbs.
  • The tremor is often ‘pill rolling’, the thumb moving rhythmically backwards and forwards on the palm of the hand.
  • It occurs at rest, improves with movement and disappears during sleep.
  • RIGIDITY is detected by examination. It predominates in the flexor muscles of the neck, trunk and limbs and results in the typical ‘flexed posture’.

BRADYKINESIA: This slowness or paucity of movement affects facial muscles of expression (mask-like appearance) as well as muscles of mastication, speech, voluntary swallowing and muscles of the trunk and limbs. Dysarthria, dysphagia and a slow deliberate gait with little associated movement (e.g. arm swinging) result.

  • Tremor, rigidity and bradykinesia deteriorate simultaneously, affecting every aspect of the patient’s life:
  • Handwriting reduces in size.
  • The gait becomes shuffling and festinant (small rapid steps to ‘keep up with’ the centre of gravity) and the posture more flexed.
  • Rising from a chair becomes laborious with progressive difficulty in initiating lower limb movement from a stationary position.
  • Eye movements may be affected with loss of ocular convergence and upward gaze.
  • Excessive sweating and greasy skin (seborrhea) can be troublesome.
  • Depression occurs in about 50%.
  • As the disease progresses the frequency of drug induced confusional states and dementia increases, with 80% developing dementia after 20 years of disease (if they survive).
  • Autonomic features occur – postural hypotension, constipation.
  • REM sleep behavior disorder – where patient acts out dreams and may hurt themselves or their sleep partner. May precede onset of motor symptoms.
  • Time of onset is mid-late fifties with increasing incidence with increasing age. Juvenile presentation can occur, when presentation and disease progression is often atypical; a genetic basis is more often found.

DIAGNOSIS

The diagnosis of PD in the early stages is difficult. Post-mortem data from the London Brain Bank shows this to be incorrect in 25% of those diagnosed in life.

  • New tremor in middle age causes particular difficulty – senile/essential & metabolic tremor generally absent at rest and worsened by voluntary movement.
  • The diagnostic use of a L-dopa or dopamine agonist (apomorphine) challenge has decline due to concerns that it may increase the risk of subsequent drug induced dyskinesia.
  • Functional imaging (SPECT & PET) should improve diagnostic accuracy and ensure that persons with conditions unresponsive to treatments (PD mimics) are not unnecessarily exposed to them.

TREATMENT

Treatment is symptomatic and does not halt the pathological process. No agents have yet demonstrated convincing neuroprotective effect.

  • Levo dopa is given with a decarboxylase inhibitor, which prevents peripheral breakdown in the liver (as in I) allowing a higher concentration of dopa to reach the blood-brain barrier (as in 2) and reduces the peripheral side effects (nausea, vomiting, hypotension).
  • Central side effects: confusion, depression, dyskinetic movements and following long-term treatment – ‘On/Off’ phenomenon.
  • Rapid onset or longer action can be achieved using dispersible or controlled-release preparations.
  • Exogenous dopa improves bradykinesia, rigidity and, to a lesser extent, tremor, but in 20% the response is poor. Dopa has relatively less effect on non-motor symptoms.
  • A new preparation of dopa is available for continuous infusion via jejunostomy in severe disease.
  • Dopamine agonists: Now used earlier in disease management, they act directly on the dopamine receptor independent of degenerating dopaminergic neurons. It is not clear if patients do better in the long term if dopamine agonists or dopa are used first. There are two types of dopamine agonists, ergot derived, including pergolide, cabergoline, apomorphine and non-ergot derived.
  • COMT inhibitors: Entacapone reduces the metabolism of levodopa and is used as adjunctive treatment. Tolcapone is an alternative that can cause hepatic toxicity; it requires close monitoring.

For you, the patient or carer, we hope our website www.branerpainclinic.com covers any question you may have regarding Parkinson’s disease in your life. However, if you can’t find quite what you’re looking for – or you would like to know more – please feel free to Contact Us at our clinic Braner Pain Clinic and Call Now : 1 (877) 573-1282. We’d be glad to help in any way we can.

How to treat Vascular Malformations in the Brain?

Investigations, Management And Treatment of Vascular Malformations:Vascular Malformations

Vascular malformations vary in size and different forms exist:

Arteriovenous malformations (AVMs) are developmental anomalies of the intracranial vasculature; they are not neoplastic despite their tendency to expand with time and the descriptive term ‘angioma‘ occasionally applied.

Dilated arteries feed directly into a tangled mass of blood vessels of varying calibre; they bypass capillaries and shunt oxygenated blood directly into the venous system. Due to high intraluminal pressure, veins may adopt an ‘aneurysmal’ appearance. Arteriovenous malformations occur at any site but are commonest in the middle cerebral artery territory.

  • Capillary Telangiectasis:  An area of dilated capillaries, like a small petechial patch on the brain surface – especially in the pons. These lesions are often only revealed at autopsy.
  • Cavernous Malformation/Angioma: Plum colored sponge-like mass composed of a collection of blood filled spaces with no intervening brain tissue. No enlargement of feeding or draining vessels.

ARTERIOVENOUS MALFORMATIONS

CLINICAL PRESENTATION

  • Haemorrhage: About 40 60% of patients with an AVM present with haemorrhage -often with an intracerebral or intraventricular component. In comparison with saccular aneurysms, AVMs tend to bleed in younger patients, i.e. 20-40 years, and are less likely to have a fatal outcome. Vasospasm and delayed ischaemic complications rarely develop. Small AVMs, those with high intranidal pressure and those draining exclusively to deep veins have an increased risk of haemorrhage.

1)      Annual Risk of Haemorrhage: Patients with no history of haemorrhage have an annual risk of bleeding of 2-4%. For those presenting with haemorrhage, the risk of re-bleeding may be higher, particularly in the first year. One study reported an annual risk of 17%.

2)      Mortality from Haemorrhage: In contrast to the high mortality following aneurysm rupture, haemorrhage from an AVM carries the relatively low mortality rate of approximately 10%.

  • Epilepsy: Generalized or partial seizures commonly occur in patients with arteriovenous malformation, especially if the lesion involves the cortical surface. Of patients presenting with haemorrhage, 30% have a history of epilepsy.
  • Neurological Deficit: Large AVMs, especially those involving the basal ganglia, may Present with a slowly progressive dementia, Hemiparesis or visual field defect, Probably as a result of a ‘steal’ effect. The infrequent brain stem AVM may also produce a motor or sensory deficit, with or without cranial nerve involvement.
  • Headache: Attacks of well localized headache – unilateral and throbbing – occur in a Proportion of patients subsequently shown to have a large AVM.
  • Cranial Bruit: Auscultation, especially over the eyeball, occasionally reveals a bruit.

INVESTIGATIONS

  • CT scan: Most AVMs are evident on CT scan unless masked by the presence of an intracranial haematoma. A double dose of intravenous contrast may aid visualization, especially with small cryptic lesions.
  • MRI: Conventional MRI will clearly demonstrate the AVM as a region of flow voids, with associated signal change within or around the lesion from areas of old haemorrhage or gliosis. The MRI provides exact anatomical detail and helps surgical Planning. Functional MRI aids identification of any adjacent eloquent areas.
  • Angiography: Both CT and MR angiography should confirm the presence of an AVM but digital subtraction four-vessel angiography is required to delineate the feeding and draining vessels. Occasionally small AVMs are difficult to detect and only early venous filling may draw attention to their presence.
  • N.B.: In the presence of a haematoma, digital subtraction angiography should be delayed until the haematoma resolves, otherwise local pressure may mask demonstration of an AVM. If the angiogram is subsequently negative, then MRI is required to exclude the presence of cavernous malformation.

MANAGEMENT

Various methods of treating arteriovenous malformations are available. All risk further damage and a team comprised of the neurosurgeon and neuroradiologist should decide on the optimal method or combination of methods for each patient. The urgency of the patient’s clinical condition and the risks of treatment must be weighed against the risk of a conservative approach.

Indications for Intervention

  • Expanding haematoma associated with AVM
  • Progressive neurological deficit
  • Risk of haemorrhage especially
  • young patients with many years at risk
  • AVMs < 3 cm

METHODS OF TREATMENT

  • Operation:  Excision – complete excision of the AVM (confirmed by per- or postoperative angiography) is the most effective method of treatment particularly for small AVMs in non-eloquent areas. Image guidance may aid localization. Larger lesions (> 6 cm) have a greater risk of postoperative hyper perfusion syndrome and brain swelling and carry a 40% risk of permanent neurological deficit.
  • Stereotactic Radio-Surgery:  Focused beams from multiple cobalt sources or from a linear accelerator (25Gy) obliterates about 75% of AVMs < 3 cm in diameter, but this may take up to 3 years during which time the risk of haemorrhage persists. In smaller lesions < 1 cm the obliteration rate with 25Gy approaches I0O%. For lesions greater than 3 cm, the lower dose required to minimize the damaging effect of local tissue destruction, makes obliteration unlikely. Pre-treatment with embolisation helps only if this produces a segmental reduction in size. Suboptimal embolisation may merely hinder radio surgical treatment. Despite the delay in action, radio surgery may prove ideal for small deeply seated lesions.
  • Embolisation: Skilled catheterization permits selective embolisation of feeding vessels with isobutyl-cyanoacrylate, although this technique is not without risk. Embolisation may cure up to 40% of AVMs when small particularly if supplied by a single feeding vessel, but filling may persist from collaterals. When used preoperatively, it may significantly aid operative removal.

If you are being affected from vascular malformation in the brain disease come instantly Braner Pain Clinic. For more detailed information Call Now: 1 (877) 573-1282

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What treatment should a person with Cervical Spondylosis do?

Clinical Features And Management of Cervical Spondylosis:Cervical Spondolysis

The mobile cervical spine is particularly subject to osteoarthritis change and this occurs in more than half the population over 50 years of ages: of these approximately 20% develop symptoms. Relatively few require operative treatment.

Resultant damage to the spinal cord may arise from direct pressure or may follow vascular impairment. The onset is usually gradual. Trauma may or may not predispose to the development of symptoms.

CLINICAL FEATURES

RadicuIopathy:

Pain: A sharp stabbing pain, worse on coughing, may be superimposed on a more constant deep ache radiating over the shoulders and down the arm.

Paraesthesia: Numbness or tingling follows a nerve root distribution.

Root Signs:

  • Sensory loss, i.e. pin prick deficit in the appropriate dermatomal distribution.
  • Muscle (I.m.n.) weakness and wasting in appropriate muscle groups.
  • Reflex Impairment / lossC5, 6….. Biceps, supinator jerk: C7……. triceps jerk.
  • Trophic Change: In long-standing root compression, skin becomes dry, scaly, inelastic, blue and cold.

Arms: l.m.n. signs and symptoms, as above, at the level of the lesion and/or u.m.n. signs and symptoms below the level of the lesion, e.g. CS lesion: deltoid and biceps weakness and wasting; reduced biceps reflex; increased finger reflex. C3/4 lesions produce syndrome of numb clumsy hands (reflecting posterior column loss).

Legs: u.m.n. signs and symptoms, i.e. difficulty in walking due to stiffness; ‘pyramidal‘ distribution weakness, increased tone, clonus and extensor plantar responses; sensory symptoms and signs are variable and less prominent.

Sphincter disturbance is seldom a prominent early feature.

INVESTIGATION

Plain X-ray of Cervical Spine

Look For:

  • Congenital narrowing of canal, loss of lordosis.
  • Disc space narrowing and osteophyte protrusion (foraminal encroachment is best seen in oblique views).
  • Subluxation Flexion/extension views may be required.

MRI: The investigation of choice. Sagittal views clearly demonstrate cord compression at the level of the disc space. Any hyper intensity within the cord on T2 weighting reflects cord damage and may correlate with the severity of the myelopathy and outcome. Axial views show cord compression and the degree of foraminal narrowing.

MANAGEMENT

1. Conservative

Analgesics/Cervical collar:  Symptoms of radiculopathy, whether acute or chronic, usually respond to these conservative measures plus reassurance. Progression of a disabling neurological deficit however demands surgical intervention. The clinician may adopt a conservative approach when a myelopathy is mild, but undue delay in operation may reduce the chance of recovery.

2. Indications for Operations:

  • Progressive neurological deficit- myelopathy or radiculopathy.
  • Intractable pain, when this fails to respond to conservative measures. This is rarely the sole indication for operation and usually applies to acute disc protrusion rather than chronic radiculopathy.

3. Operative Techniques:

(a)  Anterior Decompression and Fusion:

A core of bone and disc is removed along with the osteophyric projections. Although not essential, some insert a bone graft from the iliac crest, or a metallic cage to promote fusion. More recently prosthetic discs have become available. There is no evidence that any one technique produces better results than another.

 (b)  Posterior Approach:

Most suitable for root or cord compression from an anterior protrusion at one or two levels.

  • Laminectomy: A wide decompression, usually from C3-C7, is carried out. Appropriate for multilevel cord compression especially if superimposed on a congenitally narrow spinal canal.
  • Foraminaotomy: The nerve root at one or more levels may be decompressed by drilling awaver lying bone.

Results

Operative results vary widely in different series and probably depend on patient selection. Some improvement occurs in 50-80% of patients. Operation should be preventing progression rather than curing all symptoms.

If you are being affected by this serious disease Cervical Spondylosis. Braner Pain Clinics specialize in chronic pain management, neurology, neurological testing and disability.

You should call us if you have been advised to learn to live with pain; or have been denied compensation due to an injury for lack of medical evidence. For More Information Call Now at: 1 (877) 573-1282 

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How we cure Spinal Cord Pain Disease?

Causes , Symptoms and Clinical Features of Spinal Cord Compression:Spinal Cord and Root Compression

Disorders localized to the spinal cord or nerve roots are detailed below, but note that many diffuse neurological disease processes also affect the cord.

SPINAL CORD AND ROOT COMPRESSION

As the spinal canal is a rigidly enclosed cavity, an expanding disease process will eventually cause cord and/or root compression.

CAUSES:

Tumours

  • Primary
  • Secondary

Infection

  • Acute
  • Chronic

Disc Disease And Spondylosis

Manifestations of cord or root compression depend upon the following:

1. Site of lesion within the spinal canal: An expanding lesion outside the cord produces signs and symptoms from root and segmental damage.

  • ROOT: Lower motor neuron (l.m.n.) and sensory impairment appropriate to the distribution of the damaged root.
  • SEGMENTAL: l.m.n. and sensory impairment appropriate to segmental level. Interruption of ascending sensory and descending motor tracts produces sensory impairment and an upper motor neuron (u.m.n.) deficit below the level of the lesion. Lesions within the cord (intramedullary) produce segmental signs and symptoms.

2. Level of the Lesion: A lesion above the LI vertebral body may damage both the cord and its roots. Below this, only roots are damaged.

3. Vascular involvement: Neuronal damage from mechanical stretching is of less importance than the vascular effects. At first venous obstruction leads to vasogenic oedema, but eventually impaired arterial flow causes irreversible spinal cord infarction. Clinical findings may suggest cord damage well beyond the level of compression, implying a distant ischaemic effect from vessel compromise at the lesion site.

4. Speed of onset:  Speed of compression affects the clinical picture. Despite producing upper motor neuron damage, a rapidly progressive cord lesion often produces a ‘flaccid paralysis‘ with loss of reflexes and absent plantar responses. This state is akin to spinal shock seen following trauma. Several days or weeks may elapse before tone returns accompanied by the expected  ‘upper motor neuron signs.

CLINICAL FEATURES:

These depend on the site and level of the compressive lesion.

  • ROOT: Severe, sharp, shooting, burning pain radiating into the cutaneous distribution or muscle group supplied by the root; aggravated by movement, straining or coughing.
  • SEGMENTAL: Continuous, deep aching pain radiating into whole leg or one half of body; not affected by movement.
  • BONE: Continuous, dull pain and tenderness over the affected area; may or may not be aggravated by movement.

If you think you may be suffering from discomfort due to nerve root compression, visit your doctor now. In most circumstances, minimal discomfort can be handled through traditional treatments required by your doctor, such as treatment, physical rehabilitation, or massage therapy.Contact the experienced team of neurological specialists at Braner Pain Clinic to learn more about our clinic Contact us at: 1 (877) 573-1282

http://www.branerpainclinic.com/