Week 9 + 10 Nervous System Flashcards by Lindsey Briggs

how long does a migraine last

4 to 72 hours

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why do women more often have igraines

hormonal differences

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diagnostic criteria for migraines (need 2)

-unilateral head pain
-pulsating pain
-pain worsening with activity
- moderate or severe pain intensity
-and at least one of the following: nausea or vomiting, or both, or photophobia and phonophobia.

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chronic migraine dx, how many days

more than 15 days per month for at least 3 months

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trigeminal autonomic cephalagia

cluster headaches

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which headache occurs primarily warily in men

cluster

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uncommon headaches occur in clusters for a period of days followed by a long period of spontaneous remission
-extreme pain
-short duration

cluster headaches

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headache attack usually begins without warning and is characterized by severe, unilateral tearing; and burning, periorbital, and retrobulbar or temporal pain lasting 30 minutes to 2 hours.

cluster headache

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do cluster headaches usually happen on the same side

yes

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mild to moderate bilateral headache with a sensation of a tight band or pressure around the head. The onset of pain is usually gradual

tension HA

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sudden, transient disruption in brain electrical function caused by abnormal excessive hypersynchronous discharges of cortical neurons

seizure

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the recurrence of seizures and a type of seizure disorder for which no underlying correctable cause for the seizure can be found

epilepsy

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involve neurons bilaterally
-originate from a subcortical or deeper brain focus
-result from cellular, biochemical, or structural abnormalities of a widespread nature
-consciousness always impaired/lost

generalized seizures

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seizure with neurons only unilaterally

focal seizures

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involve neurons bilaterally

generalized seizures

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-local (focal) onset, and originate from discrete areas usually associated with structural abnormalities localized to the cortical brain tissue
-consciousness may be maintained

focal seizure

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occur when there is disruption in the balance of excitation and inhibition of electrical impulses

seizures

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long-lasting depolarization of the neuron caused by an influx of extracellular calcium that opens the voltage-dependent sodium channel. The influx of sodium generates repetitive action potentials.

invitation

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in epilepsy the sodium potassium channels allow for an influx of too much

too sodium
potassium takes too long to leace

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(phase of muscle contraction associated with increased muscle tone)

tonic phase

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(phase of alternating contraction and relaxation of muscles)

colonic phase

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This inhibition causes an interruption in the seizure discharge, producing an intermittent contract-relax pattern of muscle contractions. The intermittent clonic bursts gradually become more and more infrequent until they finally cease. At this point the epileptogenic neurons are exhausted and the neuronal membranes probably are hyperpolarized.

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seizures demand a 250% increase in
and a increase in what

ATP
increase cerebral oxygen need

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severe seizures can lead to deficient in

ATP, phosphocreatine, and glucose then occurs,
-lactate accumulates in the brain tissues

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Severe seizures thus may produce

secondary hypoxia, acidosis, and lactate accumulation, all of which are imbalances that may result in progressive brain tissue injury and destruction.

state of continuous seizures lasting more than 5 minutes, or rapidly recurring seizures before the person has fully regained consciousness from the preceding seizure, or a single seizure lasting more than 30 minutes.

Status Epilepticus

postictal state

period from when seizure ends and the patient returns to their baseline

The person is still in a postictal state

Status Epilepticus

Status epilepticus most often results from

-abruptly stopping antiseizure medications -untreated or inadequately treated persons with seizure disorders.

status epileptics medical emergency

-cerebral hypoxia -Mental retardation, dementia, other brain damage, and even death are serious threats. -Aspiration risk.

Two types of symptoms often signal an impending generalized tonic-clonic seizure:

1. an aura- a partial seizure that immediately precedes the onset of a generalized tonic-clonic seizure 2.prodroma (malaise, headache etc)- an early manifestation that may occur hours to days before a seizure

Two types of symptoms often signal an impending generalized tonic-clonic seizure:

signs that seizure is coming on

sudden uncontrollable jerking movements of one or more extremities or the entire body -Loss of postural tone -person falls to the ground and the body stiffens in an opisthotonos position with legs and, usually, arms extended;

evaluation for seizures

-health history -bloodwork (glucose, calcium, blood urea nitrogen, urine sodium, and creatinine) -EEG -CSF examination

Of all strokes, 87% are

ischemic (thrombotic or embolic) (obstruction within a blood vessel to the brain)

greatest risk factor for stroke

high BP

arise from arterial occlusions caused by thrombi formed in the arteries supplying the brain or in the intracranial vessels

thrombotic stroke

development of a cerebral thrombosis most frequently is attributed to

atherosclerosis (thickening, plaque in arteries) -inflammatory disease processes (arteritis) that damage arterial walls

Transient episodes of neurologic dysfunction (weakness, numbness, sudden confusion, loss of balance, loss of vision, sudden severe headache) resulting from focal cerebral ischemia.

Transient Ischemic Attacks (TIAs)

will people with TIA experience a stroke?

likely within the year

Involves fragments that break from a thrombus formed outside the brain or in the heart, aorta, or common carotid artery

embolic stroke

risk factor for stroke

atrial fibrillation (a fib)

Embolization is usually in the

middle cerebral artery (the largest cerebral artery).

when an area of the brain loses blood supply and becomes ischemic because of vascular occlusion (embolic or thrombotic).

Cerebral Infarction

most common cause of brain occlusion (lose of blood supple)

-Cerebral thrombi and cerebral emboli -also hypotension and atherosclerosis

when is Thrombolysis given

3-4.5 hours of onset of symptoms

if it is more than 4.5 hours and thrombolysis can't be given, what is given

antiplatelet agents are administered (Aspirin, clopidogrel, or aspirin plus extended-release dipyridamole)

the progressive failure (an acquired deterioration) of many cerebral functions that includes impairment of intellectual function with a decrease in orienting, memory, language, executive attentional functions, and alterations in behavior. The greatest risk factor is age.

dimentia

mechanisms leading to dementia

1. neurodegeneration 2. atherosclerosis 3. trauma, lesions in the cerebral convolutions 4. increased cranial pressure

leading cause of dementia and one of the most common causes of severe cognitive dysfunction in older adults

Alzheimer’s Disease (AD)

most prevalent Alzheimer’s Disease (AD)

Nonhereditary, or sporadic, late-onset AD (70% of cases) is the most prevalent form.

Late onset AD may be associated with

chromosome 19 -involved with the apolipoprotein E gene-allele 4 (apoE4).

in AD formation of neuritic plaques containing a core of amyloid beta protein, the formation of neurofibrillary tangles, and the degeneration of basal forebrain cholinergic neurons with loss of acetylcholine.

-plaques int he brain with alzheimers

in AD failure to clear plaque in the brain leads to

disruption of nerve impulse transmission, and death of neurons.

a microtubule binding protein, in neurons detaches and forms an insoluble filament called a neurofibrillary tangle, which contributes to neuronal death.

tau protein

chemistry behind loss of memory in AD

Loss of acetylcholine and other neurotransmitters

The specific diagnosis of AD is made by

postmortem examination

_____________ are used in mild to moderate AD to enhance cholinergic transmission.

Cholinesterase inhibitors (ChE-Is)

a complex motor disorder accompanied by systemic nonmotor and neurologic symptoms.

Parkinson

main disease feature Parkinson

degeneration of the basal ganglia involving the dopaminergic (dopamine-secreting) nigrostriatal pathway

are men or women more likely to have parkinsons

men

hallmark feature of parkinsons

loss of dopaminergic pigmented neurons in the substantia nigra (SN)

underactivity of the direct motor pathway (normally facilitates movement) and overactivity of the indirect motor loop (normally inhibits movement). -bradykinesia (slow movement) and rigidity

parkinsons

problems associated with parkinson

mitochondrial dysfunction -oxidative stress -abnormal folding and accumulation of alpha-synuclein -abnormal phosphorylation- dysfunction of the ubiquitin proteasome system

fibrillar intracellular eosinophilic inclusions,

Lewy bodies

Norepinephrine is thought to be neuroprotective and loss of LC neurons may be associated with a worsening of disease progression and the behavioral symptoms of PD.

symptoms appear after a 70% to 80% loss of pigmented nigral neurons and a 60% to 90% loss of striatal dopamine.

parkinsons

classic motor manifestations of PD

-resting tremor -bradykinesia/akinesia (poverty of movement) -rigidity (muscle stiffness) -postural abnormalities

is the parkinsons tremor with movement or at restq

at rest, tremor stops with mvoement

what mauls are affected with parkinsons

All striated muscles -eventually muscles of mastication (chewing), deglutition (swallowing), and articulation

Parkinson's dx symptoms

TRAP (1) resting tremor (2) cogwheel rigidity (3) akinesia, (4) postural instability

parkinsons treatment

-dopamine agonist levodopa (l-dopa) -effective in early PD but can cause motor fluctuations,“off”periods, and dyskinesia in the long term.

is a chronic inflammatory disease involving degeneration of CNS myelin, scarring or formation of plaque, and loss of axons.

Multiple Sclerosis (MS)

genetic link for MS

HLA gene

MR envrimoentla risk factors

Vitamin D deficiency, cigarette smoking, and Epstein-Barr virus infection

The first demyelinating event, or“clinically isolated syndrome”(CIS), is a single episode of neurologic dysfunction lasting greater than 24 hours that can be a prelude to MS.

does MS effect white and grey matter

yes

MS- Autoreactive T and B cells recognize myelin autoantigens and trigger inflammation in the CNS, leading to the loss of myelin sheaths and nerve conductivity and subsequently to the death of neurons

Autoreactive T and B cells recognize myelin autoantigens and trigger inflammation in the CNS, leading to the loss of myelin sheaths and nerve conductivity and subsequently to the death of neurons

classifications of MS

Relapsing-remitting, primary progressive, secondary progressive, and progressive-relapsing.

IN 2/3RDs of MS patients what marker is elevated

CSF immunoglobulin G (IgG)

MS tx

-Acute= corticosteroids. -oral and injectable disease-modifying drugs are used to decrease the number of relapses -vitamin D

affects peripheral axons and is the generalized peripheral neuropathy commonly seen

Distal axonal polyneuropathy -more sensory than motor

cause of peripheral nuropathy

diabetes mellitus alcohol abuse

the myelin or Schwann cells are affected; occurs far less frequently. Weakness is the predominant sign with far less sensory impairment

Demyelinating polyneuropathy

-autoimmune disease triggered by a preceding bacterial or viral infection -numbness, pain, paresthesias, or weakness in the limbs -acute or subacute progressive paralysis.

Guillain-Barré syndrome (GBS)

most common peripheral paralysis of the 7th cranial nerve, the facial nerve, with an onset that is rapid and unilateral

Bells Palsy

virus associated with Bells Palsy

Herpes simplex type 1

sudden, severe, brief, stabbing, and recurrent pain within the distribution of one or more branches of the trigeminal nerve that supplies the forehead, cheek, and lower jaw.

Trigeminal Neuralgia`

is Trigeminal Neuralgia bilateral or unilateral

unilateral

drug for trigeminal neuralgia

anticonvulsant drug carbamazepine.

disorders of spinal nerve roots. As the spinal roots emerge from or enter the vertebral canal,they may be injured or damaged by compression, infection, inflammation, ischemia, or direct trauma whereby the roots are stretched or torn.

Radiculopathies

clinical manifestations of radiculopathies

-Tone and deep tendon reflexes are decreased -local pain

Week 9 + 10 Nervous System Flashcards

(93 cards)