Survey
* Your assessment is very important for improving the workof artificial intelligence, which forms the content of this project
* Your assessment is very important for improving the workof artificial intelligence, which forms the content of this project
Lead Poisoning and Seizures Dayna Ryan, PT, DPT Winter 2012 Lead Poisoning Overview Normal blood lead level is “0” Toxicity is not evident until blood lead levels build up over months or years Toxic threshold is lower in children & pregnant women High levels can be fatal Lesion Site CNS or PNS In children: brain (encephalopathy with scattered hemorrhages) In adults: peripheral myelin or axon (peripheral neuropathy) Lead Poisoning Etiology In children: lead-based paint in old building (prior to 1978) Contaminated air, water, soil, toys, glazed dishware, imported canned food, cosmetics Onset After months of exposure unless large amount Faster absorption with inhalation Signs & Symptoms Muscle weakness that can progress to paralysis Atrophy of muscles Tremor Abnormal DTRs (CNS lesion ↑, PNS lesion↓) Chronic exposure in children affect UEs more, cause wrist drop Mental retardation, learning disabilities Hyperactivity, behavior problems Loss of appetite, vomiting, abdominal pain Unusual paleness from anemia Sluggishness, fatigue Fasciculations (twitches) Lead Poisoning Diagnosis Prognosis depending on Blood test Slowed motor NCVs Fibrillation potential on EMG Length & level of lead exposure Whether myelin (initial exposure) or axon (prolonged exposure) is damaged Treatments Remove the source! Chelating agents to bind the lead so that it's excreted in the urine Epilepsy / Seizure “Electrical storm in the brain” Epilepsy Chronic disorder characterized by recurrent episodes of seizures due to excessive discharge of cerebral neurons Seizure Involuntary movement or convulsions Altered mental awareness Due to excessive electrical activity in the brain Etiology Mostly idiopathic (unknown) Genetic predisposition in 1% of cases Any major disease or illness In older adults age > 50, CVA is # 1 cause Chaotic excessive electrical discharge of large aggregates of neurons in the brain Onset Mostly occur unpredictably at any time Some are provoked General Characteristics Tonic: jaw fixed, hand clenched Clonic: rhythmic jerky contractions & relaxation, biting, froth on lips Non-convulsive: changes in behaviors Classification of Seizure Partial seizure Simple partial Complex partial (most common) Generalized seizure Tonic-Clonic (i.e. Grand Mal) Absence (i.e. petit mal) **most common type Sometimes, simple or complex partial can develop into generalized tonic-clonic Simple Partial (focal seizure) Patients are conscious during seizure Unilateral hemispheric involvement, from a distinct, focal area of cerebral cortex Symptoms could be motor, somatosensory, or visual, depending on the brain area involved. Complex Partial Altered or loss of consciousness Involve bilateral hemispheres, usually temporal lobes Automatic, involuntary, repetitive behaviors Clumsy movements Confused, mumbling, pulling clothing, head turns Tonic-Clonic (grand mal) Sudden loss of consciousness & fall Tonic: generalized rigidity Clonic: very rapid generalized jerking movements Postictal: altered speech, weakness, disorientation, muscle soreness, HA Absence Seizures (Petit Mal) Sudden cessation of ongoing consciousness activity Stares into space Only minor convulsive muscle activity or loss of postural control Simple, brief, automatic movements More common in children, usually remit in adulthood Epilepsy Diagnosis Treatment History from patient & observation from bystanders EEG Identify underlying diseases, rule out other causes Education Anticonvulsants (e.g. Gabapentin) Surgery Vagal nerve stimulation – sends inhibitory signals to cerebrum Prognosis Increased mortality rates (due to underlying condition) Death from asphyxia (eating or swimming during a seizure) 20 X risks of sudden death (cardiac arrhythmia, MI) Remission = 75% in idiopathic seizure diagnosed before age 10