Test 4 Neuro Flashcards

Question

What is the hypothalamus? Where is it located? What does it do? 452

Answer 1

Small structure inferior to the thalamus, that exerts its function through the endocrine system and neural pathways Base of the forebrain/diencephalon maintain constant internal environment, implement behavioral patterns, control ANS function, regulate body temp, endocrine function (hunger etc), adjust emotional expression

Answer 2

large network of diffuse nuclei connecting the brain stem to the cortex and controls vital reflexes -cardiovascular function & respiration -essential for maintaining wakefulness and attention (consciousness)

Answer 3

group of nuclei that includes the caudate nucleus, putamen, and globus pallidus -voluntary movement and cognitive and emotional function -lecture says increase muscular tone & a primary symptom of injury to this area is increased tone

Answer 4

A bulging appearance below the mid-brain -transmits information from the cerebellum to the brainstem and between the two cerebellar hemispheres. -The nuclei from the fifth - eighth cranial nerves are located here

Answer 5

also called the myelencephalon forms the lowest portion of the brain stem. Reflex activities (HR, respiration, blood pressure, coughing, sneezing, swallowing and vomiting. Nuclei of cranial nerves nine- twelve are in this area

Answer 6

bilateral basal ganglia, corpus callosum, medial cerebral hemispheres, superior surface of frontal and parietal lobes -Hemiplegia on contralateral side -urinary incontinence -if L side may cause expressive aphasia

Answer 7

frontal lobe, parietal lobe, cortical surface of temporal lobe, Broca's area, part of occipital -aphasia in dominant hemisphere -contralateral hemiparesis (UPPER> lower) -head and eye deviation toward the side of the stroke -LEFT: aphasia, possibly global -RIGHT: possible apraxia, hemineglect Lecture and Google: SAYS VISUAL AND SENSORY

Answer 8

Part of diencephalon (thalamus, hypothalamus) temporal lobe, occipital lobe, cerebellum, parietal -visual loss contralateral -diplopia, hemianopia -sensory loss -contralateral hemiplegia if cerebral peduncle affected -aphasia

Answer 9

posterior occipital, cerebellum, brain stem, thalamus, medulla, pons hemi or quadriparesis, loss or change in vision, confusion, AMS -SWALLOW -Speech -loss of pain and temp sensation -Muscle weakness -balance/vertigo -nystagmus -N/V -diplopia

Answer 10

Paired carotid arteries

Answer 11

1. posterior cerebral arteries 2. posterior communicating arteries 3. internal carotid arteries 4. anterior cerebral arteries 5. anterior communicating arteries -collateral circulation if occlusion occurs. though 5% of the population does not have an intact COW. -assists in regulating differential blood flow to the brain -shuts blood where it's needed most based on current activity (ie thinking= frontal, running= motor cortex)

Answer 12

More permeable, increased risk for meningitis. As they get older the permeability decreases and fewer organisms can cross.

Answer 13

1. endothelial cells in the brain capillaries have intracellular tight junctions (EXCEPT at the hypothalamus to allow for sensing) 2. Only some substances: glucose, lipid-soluble molecules, electrolytes, and some chemicals can cross; is facilitated by transport molecules.

Answer 14

Outflow does not match arterial inflow. Adequacy of venous outflow can significantly affect ICP. If someone with a head injury turns their head or allows it to fall, this can partially occlude venous return causing an increase in ICP.

Answer 15

choroid plexus in the lateral, third, and fourth ventricles produce the majority of CSF. 35mL/min or about 500mL/day protection from jolts and blows, buoyant properties prevent the brain from tugging on meninges, nerve roots, and blood vessels. Tight junctions in the choroid blood vessels provide a limiting barrier between CSF and the blood similar to the BBB.

Answer 16

the total volume of the brain, cerebrospinal fluid (CSF), and blood within the cranium is constant. This means that if one of these components increases in volume, the volume of one or both of the other components must decrease. Implications in ICP management, blood is the easiest and fastest to change. High ICP may not be symptomatic initially because of adequate compensation.

Answer 17

70-90mmHg MAP-ICP=CPP 5-15mmHg, >20-25 considered Increase Intracranial Pressure or Cranial hypertension

Answer 18

1. Compensatory- vasoconstriction and external compression of the venous system occur to further decrease ICP. ----May be asymptomatic if effective. 2. Early signs- high ICP exceeds the brain's compensatory capacity. Pressure begins to compromise oxygenation, and systemic arterial vasoconstriction occurs to elevate the systemic blood pressure to sufficiently overcome the ICP. -----Symptoms: subtle and transient; episodes of confusion, restlessness, drowsiness, and slight pupillary and breathing changes. 3. Brain injury begins- ICP begins to approach arterial pressure, the brain tissues begin to experience hypoxia and hypercapnia and the patient's condition rapidly deteriorates. -----Symptoms: decreased LOC, neurogenic hyperventilation, widened pulse pressure, bradycardia, and pupils become small and sluggish. 4. Herniation- brain tissue shifts from the compartment of greater pressure to a compartment of lesser pressure. The shifted tissue's blood flow is compromised causing further ischemia and hypoxia in herniating tissues.

Answer 19

1. Uncal 2. Central 3. Cingulate/subfalcine 4. Transcalvarial/extra cranial 5. Upward herniation of cerebellum 6. Cerebellar tonsil/cerebellum into foramen magnum

Answer 20

-coordinates and maintains the steady state among body organs -regulates cardiac muscle -smooth muscle - regulation of the body's glands -sweating -piloerection -visceral reflexes

Answer 21

Cervical 8 Thoracic 12 Lumbar 5 Sacral 5 Coccygeal 1 CORD originates in the medulla and ends at the first or second lumbar vertebra in adults. Cauda equina= nerves that continue from the end of the spinal cord and form a nerve bundle. Significance: when doing things like lumbar punctures it is always a good idea to do it below the spinal cord as it is much higher risk for injury. Thus lumbar.

Answer 22

Anterior/ventral: Motor neurons (efferent). Carry motor stimuli to control skeletal muscles Posterior/dorsal: Sensory neurons (afferent). Carry sensory signals back to the brain.

Answer 23

1. Posterior column- carries fine touch sensation, two pint discrimination and proprioceptive information. 2. Anterior spinothalamic- vague touch, and pain 3. Lateral spinothalamic- vague touch and temperature perception

Answer 24

the main neuronal pathway that controls voluntary movement by connecting the cerebral cortex to the spinal cord.

Answer 25

Children -myelin develops into teenage years making recovery from injuries easier in children (plasticity) -reflexes are marker of healthy nervous system development -normal reflexes CHANGE AT FIRST YEAR Elderly -Decreased neurons, myelin and dendritic processes with synaptic connections therefore decrease in brain weight and size. CSF increases to fill the space. -Increased arteriosclerosis -Increased BBB permeability (increased risk of meningitis) -functional changes: decreased deep tendon reflex, taste, smell or color detection; sleep disturbances, memory impairment. ----These changes occur even in mentally competent people

Answer 26

Chronic, recurring type not associated with structural abnormalities, systemic disease, or trauma. 1. Migraine 2. Cluster 3. Tension

Answer 27

At least 5 attacks of a headache lasting 4-72 hours with at least two of the following characteristics: unilateral, pulsating, moderate or severe pain, and aggravation by or causing avoidance of routine physical activities. Must have at least one of the following symptoms: nausea and or vomiting, photophobia and phonophobia and not be accounted for with another diagnosis. Etiology: Combination of genetic and environmental Patho unknown Triggers: (things that decrease the threshold for headache) fatigue, oversleeping, missed meals, overexertion, weather change, stress or relaxation from stress, hormonal changes (menstruation), over stimulation (light, sounds, smells), chemicals (alcohol or nitrates). Phases: 1. Premonitory: up to 1/3 of people get it, can be up to days ahead of time when they get pre headache symptoms. 2. Aura: up to 1/3 get it, up to 1 hour duration, visual sensory or motor. 3. Headache 4. Recovery: irritability, fatigue, or depression may take hours or days to resolve.

Answer 28

One in a group of disorders called trigeminal autonomic cephalalgias (headache involving the autonomic division of the trigeminal nerve) that usually begins without warning. Sx: Unilateral (may alternate with each episode), severe, stabbing and throbbing pain. Occurs in clusters (up to 8 attacks in a day) and can last from minutes to days, followed by a long remission. Primarily in men age 20-50 Triggers: Alcohol, caffeine and smoking Patho: release of vasoactive peptides, neurogenic inflammation and pain activation.

Answer 29

Most common type of recurrent primary headache. Average onset is 20yo, associated with anxiety and depression. Etiology: Symptoms: bilateral and mild with sensation of tight band or pressure around the head with gradual onset of pain that can last from hours to days. Episodic =less than 15 days/mo Chronic = 15 or more days/mo x 3 months Triggers: NOT aggravated by physical activity, triggered by sleep disorders (insomnia) Patho: peripheral sensitization of myofascial nociceptors (not really known)

Answer 30

Aka Acute confusional state, can be acute or chronic, sudden or gradual onset. Patho: not well understood, possibly alteration in neurotransmitter availability and function. OR could be a failure in the function of neuronal networks that integrate and process sensory information. (Reticular activating system according to the lecture) Usually develops over hours to days Types: -Hyperactive -Hypoactive -Mixed -Terminal (seen in the final stages of dying)

Answer 31

Acquired deterioration and progressive failure of many cerebral functions including impairment of intellectual processes, decreasing ability in language, memory, judgement, and decision making. SLOW Cause: neuronal degeneration, compression of brain tissue, atherosclerotic vessels and brain trauma.

Answer 32

LEADING cause of severe cognitive and behavioral dysfunction in older adults. (2/3 are women!!) BOO!! Cause: exact not known, very likely genetic, many genes found to be possible especially with EARLY onset. Mechanism: -accumulation of extracellular neuritic plaques containing a core of abnormally folded beta amyloid proteins and tau protein neurofibrillary tangles - loss of neurons and synapses in cerebral cortex and hippocampus. -Atrophy with decreased overall brain weight and volume, loss of neurotransmitters. NO GOOD TREATMENT

Answer 33

Inflammation of the brain and spinal cord. -Bacterial it is primarily an infection of the pia mater, arachnoid villi, subarachnoid space, ventricular system and the CSF. -Agents: Streptococcus pneumoniae & Haemophilus influenzae type B (Hib) -How: Respiratory droplets, contact with contaminated saliva or respiratory tract secretions. Carriers of the meningococcal bacteria can pass it on but are not infected by it. -----Inhalation & crossing BBB -Symptoms: normal inflammatory symptoms + throbbing HA, severe photophobia, nuchal rigidity and positive KERNIG (inability to/pain with extension of the legs past 90 degrees) AND BRUDIZINSKI SIGNS (passive flection of the neck causes flexion in the knees) IN SEVERE CASES CAUSES PROJECTILE VOMITING WITH NECK FLEXION -Diagnosis: CSF with increased WBCs (neutrophils), positive polymorphonuclear leukocytes, low glucose and high protein.

Answer 34

Aka aseptic meningitis, limited to the meninges and no identifiable bacteria can be found in the CSF Agents: HSV 1&2, enterovirus (echo virus, coxsackievirus), arboviruses How: crossing BBB itself, spread along peripheral nerves, though transsynaptic transmission, choroid plexus epithelium or infected immune cell crossing the BBB. Symptoms: Similar to bacterial meningitis but MORE MILD Diagnosis: R/O bacterial cause

Answer 35

acute inflammation of the brain, usually of viral origin. Agent: infectious, postinfectious or AUTOIMMUNE ---MOST COMMON INFECTIOUS HSV1 ---CAN follow vaccination with live virus IF vaccine has an encephalitis component (ie mmr) Vector: MOST COMMON bug bites (tick, mosquito and flies) Symptoms: acute febrile illness with meningeal involvement. Diagnosis: CSF typically "normal" serologic studies, CBC, CT INTERESTING: There is a California viral encephalitis which is endemic!

Answer 36

Sudden, transient disruption in brain electrical function caused by abnormal excessive discharges of cortical neurons. Causes: ANY disorder that alters the neuronal environment can cause seizure. (ie congenital malformations, brain tumors, vascular disease, drug/alcohol use, trauma) ----Threshold decreased by hypoglycemia, fatigue, emotional or physical stress, fever, constipation, antipsychotics, HYPONATREMIA (like excess H2O intake) ***Lecture says Hyper & Hypo natremia can cause seizures, google agrees saying they do but they have different causes and treatments. The book says hyponatremia. ----LECTURE: HYPERNATREMIA SEIZURE= HIGH TONE/HYPERREFLEXIA, where hypo is lethargy Patho: Disruption in the balance of inhibitory and excitatory impulses. Kids: Febrile

Answer 37

a state of continuous tonic-clonic 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. Causes severe increase cerebral metabolic demand using glucose and glycogen stores leaving cells HYPOXIC --Neuronal death, injury and alteration of neuronal networks.

Answer 38

Lewy Bodies Decreased Dopamine generating cells Resting tremor Bradykinesia Postural instability Degeneration of the locus coeruleus causing decreased NOREPI -> depression and cognitive decline Primary = disease (genetic/idiopathic) Secondary= Acquired (drugs toxins, MS, cancer etc) -DRUG INDUCED IS THE MOST COMMON SECONDARY AND IS USUALLY REVERSIBLE

Answer 39

chronic immune medicated inflammatory disease involving degeneration of the CNS myelin, scarring (sclerosis or plaque formation), and loss of axons. Diffuse injury --PROGRESSIVE OR REPLAPSING AND REMITTING Cause: Autoimmune or post infectious (MONO) etiology unknown Common: women 20-40, higher in northern latitudes and those who have less sun exposure. Symptoms: MOST COMMON paresthesia of face, trunk, or limbs; weakness, impaired gait, or urinary incontinence. Vision changes.

Answer 40

acquired chronic autoimmune disease mediated by antibodies against the ACETYLCHOLINE receptor at the POSTsynaptic membrane of the neuromuscular junction. --Associated with other autoimmune diseases (RA, lupus) TYPE 2 HYPERSENSITIVITY Women 20-30, men >60 DESCENDING progressive weakness (according to the lecture) Fatigable muscle weakness which may involve ocular, bulbar (of eyes, face, mouth, throat, and neck), respiratory and limb muscles (according to the BOOK) Tx: Depends on subtype includes acetylcholinesterase inhibitors, corticosteroids & other immunosuppressives.

Answer 41

rare demyelinating disorder caused by humoral and cell mediated immunologic reaction directed at the peripheral nerves. --there is a demyelinating subtype Causes: usually within 4 weeks post respiratory or GI infection, associated with surgery, immunization, immune check point inhibitors, and infections (campylobacter, zika, COVID) Symptoms: can vary widely, from tingling and weakness to ASCENDING flaccid paralysis progressing to complete quadriplegia with respiratory insufficiency and autonomic instability. Treatment: IVIG or plasma pheresis ----Recovery is DESCENDING, takes weeks to 2 years. 20% will have residual weakness.

Answer 42

A permanent but not progressive disorder of movement, muscle tone, or posture caused by injury or abnormal development in the immature brain, before, during or after birth up to 1 yr. Lecture says: occurs before 3 yrs, 70% before birth Symptoms: spasticity, dystonia, ataxia, or a combination (mixed). Diplegia, hemiplegia, or tetraplegia. MOST COMMON PYRAMIDAL/SPASTIC ---often have associated neurologic disorders such as seizures and intellectual impairment ranging from mild to severe.

Answer 43

Parenchyma Pipes Perfusion Penumbra Prevent Complications

Answer 44

episodes of neurologic dysfunction resulting from temporary arterial obstruction of brain blood flow, does not show evidence or acute infarct on imaging. --Episodes last less than 24 hours (less than 60 minutes on the slides, about 15 minutes on google!!) Symptoms: sudden severe HA, hemiparesis, numbness, sudden confusion, loss of balance, loss of vision, speech disturbances. 17% of people with TIA will have a stroke within 3 months

Answer 45

TIA but longer and no increased risk of stroke following. Sudden deficits that reverse in more than or equal to 24 hrs (google says 7 days)

Answer 46

occlusion of a single, deep perforating artery that supplies a small penetrating subcortical vessel, causing ischemic lesions (0.5-15mm) or lacunes deep in the brain (thalamus or basal ganglia) but not the cortex --accounts for 25% of ischemic strokes --20% recurrence rate --associated with cerebral small vessel disease and UNTREATED HTN Symptoms: motor or sensory deficits due to location and small area of infarct, can also be silent Lecture: deficits progress 24-36hrs, linked to vascular dementia

Answer 47

arterial obstruction caused by thrombus formation in arteries supplying brain or intracranial vessels, MOST OFTEN FROM ATHEROSCLEROSIS. (AND INFLAMMATION lecture) Lecture: usually large vessel, ONLY type of stroke with slow progressive onset (AKA long term to make the atherosclerotic lesion?)

Answer 48

involves fragments that break from thrombus formed outside the brain, usually the heart, aorta or common carotid artery. Can also be fat, air, tumor, bacterial lumps and foreign bodies. MOST COMMON MCA Deficit worst at onset

Answer 49

Ischemic Stroke with NO identifiable underlying cause

Answer 50

MOST COMMON LOCATION: deeper parts of the brain: basal ganglia, thalamus, pons and caudate nucleus. Adjacent brain is deformed, compressed, and displaced causing ischemia, edema, increased intracranial pressure and necrosis. Expanding mass effect can cause brain stem herniation. Seepage or rupture into the ventricular system often occurs, and hydrocephalus can develop due to microscopic blood obstruction of the CSF outflow tracts. MAX cerebral edema at 72 hrs and takes 14 days to subside. Secondary injury from immune response, complement increases edema & RBC lysis, microglia/macrophages and leukocytes release inflammatory cytokines increasing inflammation. Oxidative stress increases cellular injury and death. Blood component breakdown products also promote secondary injury. Cause: HTN!!

Answer 51

bleeding between the dura mater and the arachnoid membrane covering the brain CAUSED BY TEARING OF THE VEINS MOST COMMON CAUSE OF TRAMATIC INTRACRANIAL MASS LESION (10-20%) rare cause anticoagulant therapy or vascular malformations. Rapid onset (hours) for ACUTE, slower 24hrs to 2 wks for CHRONIC CRESCENT SHAPED

Answer 52

bleeding between the dura mater and the skull. Often a result of ARTERIAL BLEED MOST COMMON SITE TEMPORAL FOSSA from -MIDDLE meningeal artery -ASSOCIATED WITH SKULL FX Biconvex shape (shape of sun just before it sets on horizon/lense) Sx: loss of consciousness at initial injury, a period of lucidity and then loss of consciousness again.

Answer 53

Bleeding into the subarachnoid space, between arachnoid and pia mater ANEURYSM RUPTURE, but can also occur after TBI from shearing forces MOST ARE MILD Looks like starfish in middle of brain (lecture says blood in circle of willis cisterns and fissures but I think it looks like a starfish)

Answer 54

Bleeding within brain tissue, may be single or multiple and are associated with contusions. Most are located in frontal and temporal lobes but may be in hemispheric deep white matter. ICH functions as an expanding mass increasing ICP, compressing brain tissues, and causing edema. 2-3% of head injuries Can be caused by stroke to tumor as well

Answer 55

involves widespread areas of the brain and occurs with all severities of brain injury. Results from mechanical effects of high level acceleration and deceleration injury such as whiplash or rotational forces that cause shearing and stretch of delicate axonal fibers and white matter tracts that project to or from the cerebral cortex. Can only officially be diagnoses at autopsy with electron microscope. Often not visible on CT, but may be seen as diffuse punctate hemorrhages in areas where axons and small blood vessels are torn. (increased visibility 12hrs to days after injury) Severity depends on force and location KIDS HAVE NORMAL CTs BUT DON'T WAKE UP FOR DAYS/WEEKS/MONTHS

Answer 56

1. Hypotension 2. Hypoglycemia 3. Hyponatremia 4. Hypoxia 5. Hypercarbia 6. HYPERTHERMIA

Answer 57

1. Post concussion syndrome-> sports --Mild TBI. --Lasts weeks - mo --HA, dizziness, anxiety, fatigue, irritability, photophobia, depression --symptom management 2. Chronic traumatic encephalopathy --> sports/repeated blast injury like soldiers, also called CTE (football) --progressive dementia --violent behavior, depression, suicide, memory loss --Diagnosis based on history and autopsy 3. Post traumatic Seizure --10-20% of TBI --can be within days or up to 5 yrs or longer after --initial treatment with antiseizure medication at time of injury for one week. Only continue if seizure occurs.

Answer 58

Initial mechanical trauma, and immediate tissue injury OR inadequate immobilization after injury. Flexion, extension, compression or rotation Grades: -Concussion: temporary disruption of cord function -Cord contusion: bruising of neural tissue causing swelling and temporary loss of function -Cord compression: pressure on cord causing ischemia- must be relieved -Laceration: tear of tissues of cord, spectrum of injury severity -Transection: severing of cord with permanent loss of function

Answer 59

Quad: C6 and above Para with arm: T6 and below Para with trunk: L1 or below

Answer 60

Fever with no other neurologic symptoms except for seizure, no CNS infection or other acute neurologic illness Temp >38 Simple: -6mo-5yrs -Duration LESS than 15 minutes -one in 24hrs -generalized -postictal with return to BASELINE Complex: -Any age -Duration GREATER than 15 minutes -Multiple seizures per 24hr period -Generalized or focal -Postictal may not fully return to baseline after multiple seizures

Answer 61

-Transduction- receptor activation -Transmission- nerve to spine to brain -Perception- (has several requirements) coordination of meaning -Modulation- facilitation or inhibition of pain signals

Answer 62

Lou Gehrig's Disease Progressive neurodegeneration of upper and lower motor neurons. Amyotrophic- progressive muscle wasting (lower neurons) Lateral Sclerosis- scarring of the spinal cord (upper neurons) Cause unknown, some contributing genetic mutations 5-10% of cases, vast majority are "sporadic" with no identifiable genetic link. More common in Caucasians, men, generally > 40yo, median on set 51-66yo.

Answer 63

temporary loss of spinal cord functions below the lesion. Spinal shock develops immediately after injury because of loss of continuous tonic discharge from the brain or brainstem and inhibition is central descending impulses. Caused: -cord hemorrhage -edema -anatomic transection Trajectory: normal activity below injury ceases Transient drop in BP bradycardia poor venous circulation loss of thermal control (lack of ability to vasoconstrict) Progresses over hours, lasts 2-3 days Takes weeks to months for return of reflexes

Answer 64

Life threatening complication of spinal injury AT OR ABOVE T6 descending inhibition is blocked Sx: -paroxysmal HTN (up to 300!!) -pounding HA -blurred vision -sweating above level of lesion -flushing of skin -nasal congestion -nausea -bradycardia Cause: MOST COMMON: bladder distention or constipation -tight clothing or shoes -pain below lesion

Answer 65

directly controls the opening of ion channels. Critical for fast synaptic transmission Rapid Response- immediate change in cellular excitability and activity. Example: Nicotinic acetylcholine receptors Glutamate Receptors GABA-A Receptors

Answer 66

upon binding with a neurotransmitter activates intracellular signaling pathways though second messengers Slower response- slower but longer lasting effects Modulate various cellular functions such as enzyme, ion channel activities and gene expression. Example: Muscarinic Acetylcholine Receptors Dopamine Receptors Serotonin Receptors

Answer 67

Brain's ability to maintain a relatively constant blood flow across a range of cerebral perfusion pressures ensuring adequate blood flow despite changes in systemic arterial pressures. Only works when CPP is 50-150, outside this range becomes less effective increasing chances of ischemia or hyperemia

Answer 68

Vasogenic Autoregulation: vasodilation/constriction Metabolic Regulation: change blood flow based on its own metabolic activity Respiratory Gas regulation: CO2 and O2 influence on vasodilation (high CO2=vasoconstriction, low O2=vasodilation to increase blood flow and O2 availability) Neurogenic Regulation: nerves in blood vessels cause vasodilation/constriction based on signaling (sympathetic/parasympathetic)

Answer 69

1. Tonic Clonic (grand Mal): stiffening and jerking 2. Absence (Petit Mal): brief staring and unresponsiveness (seonds) 3. Myoclonic: brief jerks or fast movements 4. Atonic: sudden loss of muscle tone, head drop or falling

Test 4 Neuro Flashcards

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