{"id":5302,"date":"2011-07-14T20:25:18","date_gmt":"2011-07-14T20:25:18","guid":{"rendered":"http:\/\/crashtext.org\/misc\/5302.htm\/"},"modified":"2014-12-13T01:25:08","modified_gmt":"2014-12-13T06:25:08","slug":"5302","status":"publish","type":"post","link":"https:\/\/crashingpatient.com\/medical-surgical\/5302.htm\/","title":{"rendered":"Weakness"},"content":{"rendered":"

<\/span>Definitions<\/span><\/h2>\n

Weakness<\/em> <\/strong>is the inability to carry out a desired movement with normal force because of a reduction in strength of the muscles.\u00a0 Pts often confuse the states of malaise or listlessness, <\/em><\/strong>with true weakness.\u00a0 Fatigue<\/em><\/strong> is the diminution of strength with repetitive action<\/p>\n

Paresis <\/em><\/strong>is partial or incomplete loss of contractility, while paralysis and plegia <\/em><\/strong>are complete.\u00a0 Quad is all four, para is lower limbs, hemi is one side, mono is one limb.<\/p>\n

Myelopathy<\/em><\/strong> is a lesion of the spinal cord<\/p>\n

Myopathy<\/em><\/strong> is a disease affecting muscle<\/p>\n

A spinal nerve<\/em><\/strong> is the nerve exiting the anterior horn of the cord, while a peripheral nerve<\/em><\/strong> is a nerve outside of the spinal column.<\/p>\n

Myotome<\/em><\/strong> refers to a group of muscles receiving innervation from the same segment of the spinal cord.\u00a0 Bulbar<\/em><\/strong> refers to the tongue, jaw, face and larynx.<\/p>\n

<\/span>Neuroanatomic Subunits<\/span><\/h2>\n

Cerebral<\/p>\n

Often unilateral and accompanied by deficits such as:<\/p>\n

Aphasias, agnosias (lack of awareness of deficits), apraxias (inabilities to perform complex motor actions, ie. Button a shirt).\u00a0 Always must distinguish aphasias from dysarthrias, as the latter can be brainstem or cerebellar lesion.<\/p>\n

Processes involving the brainstem or internal capsule can give weakness, basal ganglia can present as abnormal movements.<\/p>\n

The line between central\/peripheral or UMN\/LMN is the exit of the spinal nerve from the anterior horn.<\/p>\n

<\/span>Stabilizing Management<\/span><\/h2>\n

Airway and respiratory failure are the big killers.\u00a0 Circulatory collapse is also a possibility.\u00a0 Assess phonation and the ability to handle secretions.\u00a0 Tachypnea is an ominous sign (tidal volume usually disappears before upper airway collapse.)\u00a0 Pulse ox and PCO2 are poor indicators, for patients with GBS, MG, or other cause of rapid deterioration from weakness, obtain pulmonary function testing.\u00a0 FVC (forced vital capacity less 10-12 cc\/kg or a NIF (negative inspiratory force) <20 cmH2O may indicate the need for mechanical ventilation.\u00a0 These results may be thrown off by the inability of the patient to make a tight seal around the pulm. function mouthpiece.<\/p>\n

 <\/p>\n

Probably wise to avoid Sux if intubation is needed, though the risk is probably not real until 72 hours post onset.<\/p>\n

 <\/p>\n

Autonomic dystability can accompany GBS, and is often heralded by sinus tach on ekg.<\/p>\n

<\/span>History<\/span><\/h2>\n

<\/span>Unilateral<\/span><\/h3>\n

\u00b7\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0 Are cortical signs present (aphasia, agnosia, apraxia, or neglect)?<\/p>\n

\u00b7\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0 Is the face involved?<\/p>\n

\u00b7\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0 Is there a dermatomal or myotomal pattern to the weakness? Is the description of the weakness consistent with a peripheral nerve?<\/p>\n

\u00b7\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0 Is there bowel or bladder involvement?<\/p>\n

 <\/p>\n

Unilateral facial weakness is either in the brainstem or the cortex.\u00a0 Localized process suggests peripheral nerve injury.<\/p>\n

 <\/p>\n

<\/span>Bilateral<\/span><\/h3>\n

\u00b7\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0 Is mental status impaired?<\/p>\n

\u00b7\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0 Which limbs are involved?<\/p>\n

\u00b7\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0 Sensory involvement?\u00a0 Is there a level?<\/p>\n

\u00b7\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0 Bladder involvement?<\/p>\n

\u00b7\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0 Primary or Distal muscle groups?<\/p>\n

\u00b7\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0 Flucuating pattern to the weakness?<\/p>\n

\u00b7\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0 Are there associated bulbar signs?<\/p>\n

 <\/p>\n

CNS lesions will usually have a change in mental status unless in the spinal cord.<\/p>\n

A sensory level and\/or bladder involvement points towards a myelopathy.\u00a0 Proximal>distal weakness is often the sign of a myopathy.\u00a0\u00a0\u00a0 If the weakness has a fatiguing pattern, the deficit will usually be at the NMJ (neuromuscular junction.)\u00a0 Acute attacks of weakness that resolve in a few hours suggest periodic paralysis.\u00a0 Visual and bulbar involvement often indicates an NMJ problem.\u00a0 Consider occult infection or infant botulism at the extremes of age.\u00a0 Cold reversal is ciguatera poisoning.<\/p>\n

Lhermitte\u0092s sign:\u00a0 <\/strong>an electric or tingling sensation that travels down the spine and into the extremities is a common sign of MS, but can be seen with radiculopathies and vitamin B12 deficiency as well.<\/p>\n

<\/span>Physical Exam<\/span><\/h2>\n

Look for the bronze discoloration of Addison’s disease or the heliotropic, violaceous rash of dermatomyositis.\u00a0 If anything in the history suggests tick exposure, search diligently, as removal can be curative of the weakness.\u00a0 A careful neck exam for thyroid involvement can also be revelatory.<\/p>\n

<\/span>Neurologic Exam<\/span><\/h3>\n

Identify if UMN (spasticity, hyperreflexia, and extensor babinski) signs or LMN (hyporeflexia, fasiculations, hyporeflexia)\u00a0 signs.\u00a0 Initially, a UMN lesion can present with LMN signs, developing UMN later.<\/p>\n

The key to differentiating GBS and other neuropathies from myopathies and NMJ disorders when presented with bilateral LMN signs is sensory involvement.\u00a0 GBS will have sensory involvement, myopathies should have no effect other than myalgia on the sensory system.<\/p>\n

Strength Testing<\/p>\n

Rising out of a chair or stepping up on a chair is a good test for prox motor weakness.<\/p>\n

Grade strength in the involved muscles using the standard scale:<\/p>\n

0.\u00a0\u00a0\u00a0\u00a0 Paralysis<\/p>\n

1.\u00a0\u00a0\u00a0\u00a0\u00a0 Palpable or visible contraction<\/p>\n

2.\u00a0\u00a0\u00a0\u00a0 Active movement through ROM when gravity is eliminated<\/p>\n

3.\u00a0\u00a0\u00a0\u00a0 Active movement through ROM against gravity<\/p>\n

4.\u00a0\u00a0\u00a0\u00a0 Active movement through ROM through weak resistance<\/p>\n

5.\u00a0\u00a0\u00a0\u00a0 Normal<\/p>\n

Reflexes<\/p>\n

Cerebral hemisphere lesions should hace asymmetry between the sides with hyperreflexia on the affected side. \u00a0If nerve root compression is suspected, the lack of a particular reflex can indicate the level.\u00a0 Extensor babinski\u0092s must have the other toes fan out as well.<\/p>\n

Hoffman Sign<\/strong>:\u00a0 reflex flexion of the fingers and thumb.\u00a0 Elicit by holding the patients middle finger between your index and middle finger and flicking down on the distal phalanx with your thumb.\u00a0 If present, it is a sign of a UMN lesion.<\/p>\n

Clonus<\/strong>:\u00a0 test with patient in supine position with the leg flexed at the knee.\u00a0 Rapidly dorsiflex the foot and hold it in dorsiflexion, if the foot jerks, clonus is present, another UMN sign<\/p>\n

Cremasteric Reflex:\u00a0 (T12-L1) <\/strong>\u00a0stroke thigh with tongue blade and see unilateral testicular rise<\/p>\n

Anal Wink:\u00a0 (S2-S4) <\/strong>stroke skin around sphincter and see it contract.\u00a0 Absence is abnormal<\/p>\n

Fatigability<\/p>\n

Perform repetitive, sustained oculomotor testing<\/p>\n

Tone<\/p>\n

Shake forearm to observe tone of hand on wrist.\u00a0 For lower extremities have pt lie supine and relax their leg.\u00a0 Lift up the thigh, in normal patients the foot will initially lift off the bed and then settle and slide.\u00a0 In a flaccid pt, the foot will slide on the bed the entire way.<\/p>\n

 <\/p>\n

Spasticity selectively targets the flexors of the upper extremities and the extensors of the legs.\u00a0 Rigidity increases both flexors and extensors.<\/p>\n

Fasiculations<\/p>\n

Lower motor neuron sign.\u00a0 Can be differed from benign fasciculations by the fact that they occur randomly over many parts of the muscle, while the benign form is usually in the same muscle fascicle.<\/p>\n

Assessing Gait<\/p>\n

Spasticity caused by UMN lesions will result in a stiff jerky gait while walking.\u00a0 LMN lesions will give a floppy foot that slaps as the patient walks.<\/p>\n

Sensation<\/p>\n

Cortical lesions typically cause a slight loss of sensation effecting touch and proprioception more than pain.\u00a0 Stereognosis<\/em> refers to identifying objects by touch.\u00a0 Graphesthesia<\/em> is tested by tracing a number or letter in the patients palm.<\/p>\n

Assessing Psychogenic Causes of Weakness<\/p>\n

\u0093giveaway\u0094 weakness, resistance then sudden loss is common in malingerers<\/p>\n

Hoover<\/em>\u0092s<\/em> sign the test with lifting one leg while not pushing down on opposite heel<\/p>\n

A arm that drifts down without pronating is fake<\/p>\n

A paralyzed arm will swing back and forth if you shake a patients shoulders<\/p>\n

Autonomic Symptoms<\/p>\n

Horner\u0092s syndrome<\/em> (ptosis, miosis, and anhidrosis) can be seen in internal carotid dissection, though anhidrosis won\u0092t be present in this causes as the sweat innervation comes from around external carotid<\/p>\n

<\/span>Diagnostic Testing<\/span><\/h2>\n

 <\/p>\n

<\/span>Central Unilateral Weakness<\/span><\/h2>\n

<\/span>Cortical Findings<\/span><\/h3>\n

First ask whether the limbs and face on the same side are involved.\u00a0 Eyes will look towards the lesion if the frontal lobe is damaged.\u00a0 Contralateral homonomous hemianopia (losing right\/left half of vision of both eyes) which can occur anywhere along the hemispheric visual pathway.<\/p>\n

<\/span>Lacunar Syndromes<\/span><\/h3>\n

\u00b7\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0 Deep hypertensive hemorrhages or ischemic lacunar strokes can cause weakness without cortical signs.<\/p>\n

\u00b7\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0 Pure Motor Stroke-paralysis of the face, arm and leg on one side s other signs will usually localize to the posterior limb of the internal capsule or the pons<\/p>\n

\u00b7\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0 Ataxic Hemiparesis-weakness of the lower limb associated with dysmetria of the arm or leg on the same side usually will localize to the corona radiate and the anterior limb of the internal capsule<\/p>\n

\u00b7\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0 Sensorimotor Stroke-hemiparesis or hemiplegia with ipsilateral sensory impairment will be in the thalamus and adjacent internal capsule<\/p>\n

\u00b7\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0 Dysarthria (clumsy hand syndrome)-facial weakness, severe dysarthria, and dysphagia, with mild hand weakness and clumsiness found in the corona radiate and the anterior limb of the internal capsule.<\/p>\n

<\/span>Brainstem Processes<\/span><\/h3>\n

Crossed findings.\u00a0 III and IV=midbrain.\u00a0 VI and VII=pons.\u00a0 IX-XII=medulla.\u00a0 Most likely due to vertebrobasilar circulation stroke.<\/p>\n

\u00b7\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0 Weber-midbrain, ipsilateral 3rd nerve palsy and contralateral hemiparesis<\/p>\n

\u00b7\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0 Millard-Gubler-pons, ipsilateral facial palsy, contralateral hemiparesis<\/p>\n

\u00b7\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0 Foville\u0092s-pons, ipsilateral facial paresis, abducens palsy, contralateral hemiparesis<\/p>\n

<\/span>Brown-Sequard Syndrome<\/a><\/span><\/h3>\n

<\/span>Radiculopathies<\/span><\/h3>\n

Diseased condition of the spinal roots<\/p>\n

Will almost always be in the cervical or lumbosacral distributions<\/p>\n

<\/span>Plexopathies<\/span><\/h3>\n

Lesion of a nerve plexus is identified by found by the presence of motor and sensory deficit involving more than one nerve.<\/p>\n

<\/span>Peripheral Nerve Processes<\/span><\/h3>\n

Most often neurapraxias, a temporary insult to a nerve which resolves when compression is relieved.\u00a0 Median nerve entrapment is the most common, Tinel\u0092s sign (percussion directly over the median nerve at wrist) is not useful.\u00a0 Phalen\u0092s is also fairly useless.\u00a0 Hand elevation test is better.\u00a0 Simply have the patient raise their hands over their head until the symptoms reoccur, if in median nerve distribution, then you have your diagnosis.\u00a0 Steroids are probably better than NSAIDs.<\/p>\n

 <\/p>\n

Saturday Night palsy is from compression of the radial in the axilla or along the humerus.\u00a0 Loss of grip strength which is restored with passive wrist extension.<\/p>\n

Peroneal nerve compression from crossed knees or the straps of high heels can cause foot drop.<\/p>\n

<\/span>Central Bilateral Weakness<\/span><\/h2>\n

<\/span>Central\/Brainstem Lesions<\/span><\/h3>\n

Will usually present with diminished consciousness unless localized to spinal cord.\u00a0 A lesion in the intrahemespheric fissure is more likely than bilat symmetrical cortical lesions.\u00a0 A tiny lesion in the decussation of the pyramids (cruciate paralysis of Bell) can give bilateral upper extremity weakness with no involvement of the legs.<\/p>\n

\u00b7\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0 Locked-in-pons, quadriparesis with paralysis of horizontal eye movements and everything else.\u00a0 Only vertical eye motions preserved.\u00a0 Must diagnose early as there is a chance of recovery if the basilar artery is recanalized within 12 hours.<\/p>\n

<\/span>Myelopathies<\/span><\/h3>\n

Bilat extremity weakness and sensory deficits.\u00a0 Typically the legs are involved, though cervical pathology can give this in the arms.\u00a0 There may be bowel and bladder involvement.\u00a0 Acute disruptions suggest vascular cause, while more chronic symptoms can be inflammatory.\u00a0 The most important point in this disorder is to recognize it and then rule out epidural compression syndrome.\u00a0 If it is strongly suspected, call spine surgeon and give dexamethasone (10-100 mg IV).<\/p>\n

 <\/p>\n

<\/span>Acute transverse myelitis<\/a><\/span><\/h2>\n

 <\/p>\n

<\/span>Peripheral Neuropathies<\/span><\/h2>\n

Often heralded by paresthesias and vibratory sense is almost always lost<\/p>\n

<\/span>Guillain-Barre<\/a><\/span><\/h3>\n

<\/span>Ciguatera Toxin<\/a><\/span><\/h3>\n

<\/span>Heavy Metal Polyneuropathy<\/span><\/h3>\n

Not from bad music.\u00a0 Most notable is lead<\/p>\n

<\/span>Myopathies<\/span><\/h2>\n

Almost always proximal>distal effects.\u00a0 Usually only sensory is muscle aches.<\/p>\n

<\/span>Polymyositis\/Dermatomyositis<\/span><\/h3>\n

Inflammatory myopathies causing progressive proximal muscle weakness.\u00a0 Can also progress to dysphagia and respiratory failure.\u00a0 There is no sensory loss or effect on reflexes.\u00a0 Mostly women are effected, dermatomyositis can also hit children.\u00a0 ESR and CPK will be elevated.<\/p>\n

<\/span>Electrolyte-Induced Weakness<\/span><\/h2>\n

Most commonly associated with potassium, but any significant lytes disturbance can cause weakness.<\/p>\n

<\/span>Hyperkalemic Periodic Paralysis<\/span><\/h3>\n

Autosomal dominant.\u00a0 Precipitated by exercise or cold exposure.\u00a0 Hyperkalemia is often not present during attacks.<\/p>\n

<\/span>Hypokalemic Periodic Paralysis<\/span><\/h3>\n

Can be familial or Thyrotoxic.\u00a0 Weakness is often confined to the limbs, though facial or respiratory weakness can occur as well.\u00a0 Hyporeflexic during attacks.\u00a0 Sensory exam is objectively normal.\u00a0 Rhythm monitoring may show PVCs or other disturbances.\u00a0 Attacks usually last 3-4 hours.\u00a0 Administering potassium will attenuate the attack, but should be done cautiously as whole body potassium is not low in this disorder.<\/p>\n

Famililial<\/p>\n

Usually occur during sleep or after exercise (?)\u00a0 Usually start during the second decade of life.\u00a0 Will not have onset after age 30, so think thyroid.<\/p>\n

Thyrotoxic<\/p>\n

Often affects Asians with thyroid disease.\u00a0 Increases NaK ATPase causing influx of K into cells.\u00a0 Since pumps are also activated by insulin, heavy carb meals will also cause attacks. Better strategy than replacing potassium in these patients is to give propranolol 1mg IV q10 min x 3.<\/p>\n

 <\/p>\n

\"\"<\/a> (The American Journal of Emergency Medicine\u00a0 Volume 21, Issue 6 , October 2003, Pages 487-491)<\/p>\n

 <\/p>\n

Can treat with low dose KCl (<10 meq an hour) which will hasten recovery but also increase risks of rebound hyper-K (The American Journal of Emergency Medicine 22(7):544-547)<\/p>\n

 <\/p>\n

Non-selective b-blockers can also be used<\/p>\n

 <\/p>\n

(JEM 2009)<\/p>\n

The differential diagnosis of a combination of hypokalemia, normal pH and sodium, limb weakness, and a periodic pattern after eating binges is thyrotoxic periodic paralysis (TPP), familial hypokalemic periodic paralysis (FPP), or sporadic periodic paralysis (SPP). All three usually present with a hypokalemic paralysis after ingestion of large amounts of salted or sweet foods. However, if it’s the first episode, other causes of hypokalemic paralysis must be considered. These include barium poisoning, toluene exposure, renal potassium wasting, mineralocorticoid excess (hormonal or licorice induced) and gastrointestinal losses. An excellent clinical algorithm is available in an article by Lin et al. (6).<\/p>\n

Unfortunately, the symptoms of thyrotoxicosis are often not present at the initial presentation of TPP, so thyroid function studies may be necessary to make the diagnosis if it’s the first attack ([1] and [5]). It is helpful if the symptoms of hyperthyroidism were present before the attack, or if there is a clear family history suggestive of FPP (which can be sporadic but is usually inherited as an autosomal dominant trait, with much higher penetrance in men).<\/p>\n

The emergency treatment of TPP, SPP, and FPP is initially<\/em> the same. Usually the attack will resolve spontaneously without any intervention, so observing the patient with continuous cardiac monitoring, pulse oximetry, and frequent muscle strength checks is often adequate treatment (2). Decompensation leading to stridor and respiratory failure or cardiac dysrhythmia can occur suddenly, so close observation is mandatory.<\/p>\n

Because the cause of the hypokalemia is a shift of potassium into the muscle cells, there is usually no need to replace serum potassium unless the patient has these life-threatening symptoms. A tachycardia and elevated blood pressure are the most sensitive signs of TPP and increase the possibility of TPP over FPP or SPP (7). If TPP is the most likely diagnosis, propranolol, rather than potassium, is the treatment of choice ([7] and [8]). This avoids the danger of rebound hyperkalemia, which occurs in 30\u009645% of TPP patients treated with potassium ([7] and [8]). Although there are no controlled studies demonstrating that potassium terminates the attack and there is no correlation between potassium dose and recovery time, potassium is usually administered if there is severe weakness, dysrhythmia, stridor, or respiratory failure ([5] and [8]).<\/p>\n

If potassium treatment is necessary, it is preferable to administer the potassium orally as KCl at .2\u0096.4 mmol\/kg every half-hour while following the EKG, serum potassium, and muscle strength (2). If potassium must be administered intravenously due to vomiting or inability to swallow, KCl can be administered in small boluses of .1 mmol\/kg while monitoring the EKG continuously. Because sodium or dextrose infusions can reduce the serum potassium in these patients, D5 and saline solutions should be avoided. Mannitol is the preferred vehicle if a dilute infusion of KCl (20\u009640 mml\/L) is the elected therapy (2). Great care must be exercised because rebound hyperkalemia can occur as the attack subsides and the potassium returns to the serum from the muscle cells.<\/p>\n

Repeated episodes of FPP, SPP, or TPP can result in serious interattack muscle weakness that is permanent, so long-term follow-up is necessary. An elevated creatine kinase reflects the ongoing muscle damage and pain that occurs in some patients with periodic paralysis ([8], [9] and [10]). It has been shown that hypokalemia can cause rhabdomyolysis and that may well be the mechanism for the myopathy ([11] and [12]).<\/p>\n

Preventing further episodes can be as simple as avoiding high sodium, high carbohydrate meals, or it may require treatment with the carbonic anhydrase inhibitors acetazolamide (125\u00961000 mg\/day in divided doses) or dichlorphenamide (50\u0096200 mg\/day). Because serious mental status changes can occur with these drugs, and acetazolamide may actually make the attacks worse in some patients, triamterene (25\u0096100 mg\/day) or spironolactone (25\u0096100 mg\/day) may be used instead (13).<\/p>\n

 <\/p>\n

<\/span>References<\/span><\/h3>\n

 <\/p>\n

1 R. Stedwell, K. Allen and L. Binder, Hypokalemic paralyses: a review of the etiologies, pathophysiology, presentation, and therapy, Am J Emerg Med<\/em> 10<\/strong> (1992), pp. 143\u0096148. Article<\/strong> | PDF (841 K) | View Record in Scopus | Cited By in Scopus (72)<\/p>\n

 <\/p>\n

2 R.H. Brown and J.R. Mendell, Muscular dystrophies and other muscle diseases. In: E. Braunwald, S.L. Hauser, A.S. Fauci, D.L. Longo, D.L. Kasper and J.L. Jameson, Editors, Harrison’s online<\/em>, McGraw-Hill, New York (2001), p. 50.<\/p>\n

 <\/p>\n

3 V. Sansone, T. Links, G. Meola and M.R. Rose, Treatment for periodic paralysis (Protocol), Cochrane Database Syst Rev<\/em>(2004) 3.<\/p>\n

 <\/p>\n

4 A. Chan, R. Shinde and C.C. Chow et al.<\/em>, Hyperinsulinaemia and Na+, K+-ATPase activity in thyrotoxic periodic paralysis, Clin Endocrinol<\/em> 41<\/strong> (1994), pp. 213\u0096216. Full Text<\/strong> via CrossRef | View Record in Scopus | Cited By in Scopus (43)<\/p>\n

 <\/p>\n

5 P.K. Ober, Thyrotoxic periodic paralysis in the United States, report of 7 cases and review of the literature, Medicine<\/em> 71<\/strong>(1992), pp. 109\u0096120.<\/p>\n

 <\/p>\n

6 S. Lin, J. Chiu, C. Hsu and T. Chau, A simple and rapid approach to hypokalemic paralysis, Am J Emerg Med<\/em> 21<\/strong> (2003), pp. 487\u0096491. Article<\/strong> | PDF (70 K) | View Record in Scopus | Cited By in Scopus (12)<\/p>\n

 <\/p>\n

<\/span>Neuromuscular Junction Processes<\/span><\/h2>\n