Neuro Disorders- Parkinsons, CP, MS
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Created by:
little_sam on February 29, 2012
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Terms | Definitions |
|---|---|
 Parkinsons Disease Stats | Degenerative Diseases Parkinson Disease Occurs after age 40 Mean onset 58 - 62 years Males have a higher incidence Primary CNS disorder Leading cause of neurological disability in people 60 years or older 500,000 affected in the US |
| History of Parkinsons | Degenerative Diseases Parkinson Disease James Parkinson, 1755-1824 Produces abnormal movement Disorder of the basal ganglia Alteration in the dopamine-secreting "nigrostriatal pathway" Loss of dopamine-secreting neurons(they die) |
| Possible Causes of Parkinsons | Degenerative Diseases Parkinson Disease Parkinson's 10 - 15% inherited Secondary Parkinson disease - Caused by other factors Toxins Drugs - recreational drugs (MPPP) A synthetic opioid drug MPPP when produced can have MTPT as an impurity(self induced parkinsons) MPTP causes degeneration of the substantia nigra region Secondary Parkinson disease - Caused by other factors Virus (influenza) after world war II (1920s) Influenza pandemic - increases in PD Contact with large numbers of people Free radicals PD patients appear to have enhance free radical levels Age may predispose substantia nigra region increase sensitivity to damage(older higher incidence of parkinsons) Toxins have been implicated |
| Major disease feature of parkinsons | Degenerative Diseases Parkinson Disease Major disease feature Degeneration of dopaminergic nigrostriatal pathway Damage in neurons remaining in the substantia nigra appears as Intracytoplasmic eosinophilic inclusions Lewy body (round bodies found in vacuoles) Loss of dopamine receptors (D1) in the basal ganglia Severity of the disease depends on the number of neurons damaged in the substantia nigra |
| Pathophys of Parkinsons | Degenerative Diseases Parkinson Disease Pathophysiology Loss of dopamine (NT) - inhibitory function Imbalance between excitatory and inhibitory NTs Excessive acetylcholine (excitatory NT) because of a loss of inhibition(dopamine) Resulting in Hypertonia (tremor and rigidity) Akinesia (temp loss of muscle movement) Bradykinesia (slow movement) |
| Parkinson's Symptoms | Degenerative Diseases Parkinson Disease Pathophysiology Symptoms appear after 60 - 90% of dopamine secreting neurons are damage at the nigra region Symptoms (classic) - all are present Tremor Rigidity (muscle stiffness) Akinesia (poor movement) Postural abnormalities |
| Parkinson's Tremor | Tremor Asymmetric, regular and rhythmic tremor(one sided) Late phase of the disease tremor increases in frequency and amplitude |
| Parkinson's- Postural abnormalities | Postural abnormalities Due to loss of postural reflexes Postural fixation - unable to maintain upright position Equilibrium problems Disorders in righting (correcting posture) |
| Parkinson's-neuroendocrine aspect | Neuroendocrine Basal ganglia influences hypothalamus Activation of the hypothalamus - pituitary pathway Results in excessive androgen secretion Sebum secretion - oily skin Cognitive symptoms Endogenous depression (due to pathological factors) |
| Parkinson's Treatment | L - dopa (levodopa) - precursor to dopamine Dopamine is too large to cross the blood brain barrier Anticholinergic drugs inhibit acetylcholine(suppresses excitation) Substantial side effects from these drugs and are used during later stages of the disease Fetal cell implants (dopamine secreting neurons)- improve but do not last long Stem cells may also be useful- may make dopamine receptors and inject into brain |
| Surgical Treatments-parkinsons | Previous surgical methods destruction of pathways to reduce tremor Pallidotomy- globus pallidus- has bad side effects Thalamotomy-thalamus Deep Brain Stimulation (DBS) No destruction of brain regions |
| Deep Brain Stimulation | Impulse generator Electrode surgically implanted Generator implanted under the skin Patient can actived/deactivated External magnet If tremor gets worse can activate it Current disrupts the excitation and inhibition imbalance Electrode delivers small current Blocks disruptive signals causing tremor Adjust current to optimize suppression of tremor |
| Multiple Sclerosis- Stats | Degenerative Diseases Multiple Scelerosis (MS) Onset 20 - 50 years (peaks age 30) Male/female ratio (1:2) Leading neurologic disability in younger adults Major abnormal physiology Demyelination of CNS neurons |
| Optic Symptoms-MS | Degenerative Diseases Multiple Scelerosis (MS) Symptoms - mixed (general) type Optic neuritis (optic nerve demyelination) Impaired central vision Blurring, fogginess, haziness Impaired color vision Regions of diminished vision Defective pupillary reaction |
| NS Symptoms-MS | Degenerative Diseases Multiple Scelerosis (MS) Symptoms - mixed (general) type Brain stem related symptoms Internuclear ophthalmoplegia Lateral gaze paralysis Spinal involvement Cerebellar involvement- involved in movement and memory of movement |
| Pathophys-MS | Degenerative Diseases Multiple Scelerosis (MS) Pathophysiology Suggested viral infection (immune challenge) or stress (pregnancy) occurs in patients that are genetically predisposed to MS Resulting in an abnormal immune response in the CNS T-lympocytes produce antibodies to a single myelin membrane protein Patients have elevated IgG in CSF- have crossed the blood brain barrier for some reason and caused damage in the NS |
| Sequence of Events- MS | Degenerative Diseases Multiple Scelerosis (MS) Pathophysiology (continued) Demyelination process and nerve fiber loss due to axonal break Sequence of events of MS Interaction between the systemic immune system and the CNS (autoantibodies) Demyelinating lesions (plaques occur)- antibodies attack patients own myelin |
| Molecular Level Pathophys-MS | Immune cells damage the myelin sheath Glutamate is released Glutamate binds to receptors on the oligodendrocytes "Oligos" - glial cells producing myelin in the CNS Glutamate accumulates within the glial cells Excessive excitation of the cells- leads to cell stress, damage, or death Communication along the neuron is gone |
| Treatment | Directed at acute management and reducing relapse frequency Steroid hormones - adrenocorticotropic steroids Suppress the immune responses "Copaxone"(glatiramer acetate) "decoy" protein analog of myelin Autoantibodies bind to decoy protein and protect myelin NEW TREATMENT- Betaseron |
| Betaseron | Betaseron = synthetic interferon 1b Reduces relapse and severity Less damage to neuronal tracks Side effects- flu-like symptoms |
| Betaseron Mechanism | Betaseron = Interferon (IFNs) = cytokines Activates immune system-inhibits viral infections and is ant-iinflammatory Inhibits blood brain barrier leakage-prevents leakage of antibodies into the brain Suppresses anti-myelin T-cells(suppresses cells that make autoantibodies that cause myelin destruction) Some antigens stimulate release of IFNs(interferons) |
| Cerebral Palsy- stats | 800,000 adults/children in the US 10,000 babies develop CP in the US Treatments/prevention have not improved these numbers (30 years) |
| Symptoms- CP | General Symptoms (children) Ataxia = lack of muscle coordination Spasticity = stiff/tight muscles Variations in muscle tone Hypertonia- stiff/rigid Hypotonia- relaxed or limp Difficulties in swallowing/speaking/drooling Tremor or random involuntary movement Difficulties in precise movements (eg. writing) |
| RIsk Factors for CP | Low birth weight and premature birth multiple births Infections during pregnancy Blood type incompatibility Toxic substances Maternal thyroid abnormalities or seizures Breech birth Complicated labor/delivery Low apgar score (assess fetal development) Jaundice- high fetal bilirubin levels Highly neurotoxic Seizure |
| 4 Types of Damage to brain- CP | Four types of brain damage cause symptoms Periventricular leukomalacia- damage to white matter or neuronal tracts of the brain Cerebral dysgenesis- abnormal congenital development of brain Intracranial hemorrhage- intracranial bleeding Hypoxic-ischemic encephalopathy- lack of oxygen |
| paraventricular leukomalacia | Periventricular leukomalacia White matter - CNS signal transmission pathways disrupted During development damage can occur Maternal or fetal infection Injury during development- trauma or drugs |
| cerebral dysgenesis | Cerebral dysgenesis Factors interfering in fetal development Mutation in genes regulating development Infections Fevers Traumas |
| Intracranial hemorrhage | Intracranial hemorrhage Factors leading to fetal stroke Blocked or damaged blood vessels Maternal hypertension Materanl pelvic inflammatory disease |
| Hypoxic Ischemic encephalopathy | Hypoxic-ischemic encephalopathy Factors reducing oxygen Interruption in breathing (parturition) Low maternal BP Rupture of uterus Detachment of placenta Umbilical cord problems |
| Diagnosis of CP | Diagnosis - imaging identify damage Cranial ultrasound Computed tomography (CT) scan Magnetic resonance imagin (MRI) |
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