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Physiology 2 > Neuroscience Primer > Flashcards

Neuroscience Primer Flashcards

1
Q

basic structure

A

-Brain derived from 5 embryonic regions of Neural Tube
-Telencephalon: cortex and subcortical nuclei – very front edge of the developing neural tube
-Diencephalon: thalamus and hypothalamus
-Mesencephalon: “midbrain”/quad. Plate (Superior calliculi and inferior caliculi which deal with visual and auditory reflexes)
-Metencephalon: pons and cerebellum – consciousness
Myelencephalon: medulla oblongata

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2
Q

primary vs association

A
  • Primary cortex is (in the context of sensory fxn) – receives raw data from the environment
  • Ex) what do we see? Light, wavelengths, lines, shapes – this is primary data – received in primary visual cortex
  • Then the cortex compares set of primary data to associations to things you have formed over time
  • Primary cortex has to communicate with association cortex which is typically nearby
  • Is there a single cell that lights up when you are exposed to one stimulus? NO!! Is there a network of cells
  • The more exposure you have to a particular stimulus, the stronger the network is that allows you to retrieve the information
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3
Q

occipital, temporal, post-central gyrus, and pre-central gyrus

A
  • Occipital = vision
  • Temporal = Auditory/Language
  • Post-central Gyrus = Primary Somatosensory Cortex
  • Pre-Central Gyrus = Primary Motor Cortex
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4
Q

broca’s/wernicke’s areas

A
  • Brocas = motor (tail end) (The face, larynx, and mouth is located there)
  • Wernickes = where we put meaning to words (WORD SALAD if this area is damaged)
  • You lose syntax – this may be subtle (i.e. nouns are all messed up)
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5
Q

Aphasia

A
  • “Fluent Aphasia” – Words are easily spoken but are incorrect or unrelated to content of other words. AKA Sensory, receptive or Wernicke’s aphasia.
  • “Non-fluent Aphasia” – great difficulty speaking but context and content of the words is correct. AKA motor, expressive or Broca’s aphasia.
  • Fluency = ability to form words
  • Don’t memorize what sensory or receptive refers to – he will give you fluent or non fluent
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6
Q

vasculature of the brain

A
  • Cortex fed by three major arteries: anterior, middle and posterior cerebral off the Circle of Willis
  • “Watershed” areas of vascularization most sensitive to loss of perfusion, even transient (Relies on two areas of perfusion in order to have adequate ventilation)
  • Both Wernickes and Brocas areas are in watershed regions which makes them highly susceptible to damage and thus pathology
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7
Q

subcortical nuclei

A
  • Basal Ganglia

- Amygdaloid Nucleus – involved in the aggressive behavior

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8
Q

basal ganglia

A
  • coordination of movement
  • Globus Pallidus
  • Caudate Nucleus
  • Putamen (caudate + putamen = neostriatum)
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9
Q

role of the basal ganglia

A
  • Wilson: the basal ganglia “maintain a postural background for voluntary activities.” (Don’t think of posture as standing still)
  • Reflects the primary function of the evolutionarily newer corticospinal system, making the “extrapyramidal” pathways subordinate to the cortex
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10
Q

diencephalon

A
  • Thalamus: afferent relay for virtually all sensory information (except olfaction)
  • Hypothalamus: “set points”, control of homeostatic systems of the body through pituitary gland
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11
Q

mesencephalon

A
  • Primary occupant: corpora quadrigemina (ie quadrigeminal plate (Superior colliculus: visual reflexes, Inferior colliculus: auditory reflexes
  • The cortex is NOT FAST!!! Has to think about stuff all the time
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12
Q

metencephalon

A
  • Pons: bridge of fibers to the cerebellum and container of pontine nuclei of the RAS and other systems
  • Cerebellum: control of balance and coordination of movement
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13
Q

Myelencephalon

A

-Medulla oblongata: responsible for the maintenance of vital bodily functions, very sensitive to trauma

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14
Q

Spinal cord

A
  • Butterfly-shaped central gray contains cell bodies
  • Surrounding white contains bundles of myelinated fibers
  • Dorsal and ventral roots emanate from lateral surface (anterolateral and posterolateral sulcus) forming 31 pairs of spinal nerves
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15
Q

Spinal gray matter

A

-Each spinal segment contains posterior and anterior horns, lateral horns in thoracic region

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16
Q

Spinal white matter

A

-Three paired funiculi: posterior, lateral, anterior

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17
Q

Posterior funiculus

A
  • long ascending and short (spinal ganglia) descending fibers
  • Carry proprioceptive fibers – these are posterior columns
  • They carry vibratory sensation as well
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18
Q

Lateral funiculus

A
  • lat. corticospinal, rubrospinal, lat. spinothalamic, spinotectal, spino-olivary, ant. spinocerebellar tracts
  • Spinothalamic = spinal cord to thalamus
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19
Q

anterior funiculus

A

-vestibulospinal, reticulospinal, ant. spinothalamic, tectospinal, ant. corticospinal tracts

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20
Q

ascending spinal tracts

A
  • SENSORY INFO!!! – segregated so that all the levels climb together
  • Modalities segregated so that impulses concerned with pain, temperature, touch and proprioception from various segments ascend together.
21
Q

Posterior funiculi

A

-tactile senses to the cortex (some spinocerebellar input). Lesions abolish tactile or kinesthetic senses ipsilaterally

22
Q

Anterior spinothalamic tracts

A

-cross within the spinal cord to deliver information about “light touch.” Injury produces little disturbance in tactile senses due to redundancy with posterior columns.

23
Q

lateral spinothalamic tracts

A

-pain and thermal senses. Fibers cross at segment of entry. Great clinical importance: lesion produces complete loss of pain and thermal sense from opposite side of body (not viscera).

24
Q

Spinocerebellar

A

-crossed (anterior) and uncrossed (posterior) tracts conveying positional information

25
Q

dissociated sensory loss

A
  • A regional sensory loss that involves one or two modalities, with sparing of others.
  • Example: loss of pain and temperature with sparing of positional/tactile input
  • Occurs with brainstem/sc lesion targeting spinothalamic or posterior columns or selective peripheral neuropathy targeting small unmyelinated or large myelinated fibers
26
Q

descending tracts

A
  • corticospinal
  • tectospinal tract
  • rubrospinal
27
Q

ascending tracts

A
  • posterior funiculi
  • anterior spinothalamic tract
  • lateral spinothalamic tract
  • spinocerebellar
28
Q

brown-sequard syndrome

A

-Hemisection of the spinal cord produces loss of pain and thermal sense on the contralateral side and loss of sense of position and movement on the ipsilateral (inferior to the lesion).

29
Q

upper motor neuron

A
  • All neurons which can modify the function of lower motor neurons
  • Most clinicians equate solely with corticospinal tracts (ie exclude extrapyramidal)
  • Lesions produce paralysis, disturbed muscle tone and altered reflexes, usually over broad area
  • Damage associated with Babinski sign after variable period (pathophysiology not known)
30
Q

lower motor neuron

A
  • Refers to anterior horn cells and their axons innervating striated muscle
  • AKA “Final common motor pathway”
  • Loss of AH cells leads to weakness, paralysis, loss of muscle tone and reflexes as well as atrophy of target muscles (Lose functionality on the same side as injury because the motor fibers have already crossed)
31
Q

clonus

A

Spasmodic alteration of muscular contractions between antagonistic groups – caused by hyperactive stretch reflex (UMN)

32
Q

rigidity

A

Constant resistance to passive stretch, independent of velocity of movement, resulting in “lead pipe” phenomenon.

33
Q

spasticity

A

Transient, velocity dependent resistance to passive stretch followed by relaxation.

34
Q

clasp knife phenomenon, lead pipe rigidity, cogwheel rigidity

A
  • “Clasp knife phenomenon”- Another term for spasticity, resistance varies with velocity of stretch (UMN)
  • “Lead pipe rigidity”- Constant resistance to passive stretch throughout range of motion. (Parkinsonism)
  • “Cogwheel rigidity”-Typically seen at the wrist when a resting tremor is superimposed on a “lead-pipe” rigidity. (Parkinsonism)
35
Q

pronator drift

A

-Pronator Drift: Patient extends and adducts arm in supine position, closes eyes and is distracted by shaking head “no.” Positive sign is the subtle pronation, abduction and internal rotation of the arm. (UMN)

36
Q

truncal sensory level

A
  • A dermatomal level on the trunk below which all sensation is diminished. Most often caused by a focal spinal cord lesion, most commonly thoracic.
  • Important indicator of level of spinal cord injury when symptoms suggest one exists.
37
Q

ptosis, miosis, anhidrosis

A
  • Ptosis – drooping of eyelids
  • Miosis – nearsightedness
  • Anhidrosis – lack of sweating, tears, etc.
  • “Horner’s Syndrome” – Indicates loss of sympathetic control of the face. Localizes lesion between hypothalamus and cervical sympathetic ganglia
  • Sympathetic exits spinal cord thoracolumbar
38
Q

parkinsonism

A

Basal Ganglia Circuitry (Basal ganglia run postural background for whatever activity it is that you’re doing – they carry out a motor plan until you adjust it)

  • Substantia Nigra Input – loss of cells. The cells contain melanin
  • Role of Dopamine, loss of inhibition – inhibition controls the posture
  • Pharmacology: Anticholinergics, Dopamine replacement (LDOPA), Dopamine agonists (bromocriptine or pergolide), selegiline, amantadine (About every 7 years, these meds tend to wear off, Hall marks of parkinsonism = tremors at rest)
39
Q

Characteristics of parkinsonism

A
  • Tremor at rest – fairly well defined frequency (pill rolling behavior)
  • What is a tremor? – involuntary movement and loss of posture (LOSS OF POSTURAL CONTROL!!!)
  • “Festinating” gait – small steps, shuffling
  • What does the basal ganglia do? – manages postural background for whatever activity youre doing. Whats happening if theres a change in the background? The cortex gets involved (If you have to navigate a doorway, the cortex has to get involved)
  • Don’t need to memorize this chart
  • Bradykinesia
  • Rigidity (Cogwheel)
  • Postural Disturbance
  • Dulling of affect common – masked fascies
  • If you’re asked on a test: tremor, bradykinesia, rigidity are the three classic signs of parkinsonism
40
Q

essential tremor

A
  • Brainstem and cerebellar abnormalities – NOT basal ganglia;
  • Theoretically a loss of inhibition from cerebellum modulating movement/posture;
  • Tremor may be accentuation of oscillating reflexes at spinal level in the context of loss of inhibition;
  • Inferior olivary nucleus in brainstem theorized as source of signals (target of cerebellum)
  • We also get inhibitory signals from the cerebellum!!
41
Q

tremors differential

A

isolated chin, cerebellar, voice, orthostatic, psychogenic

42
Q

med effect differential

A
  • Antidepressants, beta agonists, Depakote, Dopamine, lithium, theophylline, thyroid, etc
  • Are they overmedicated with their thyroid meds or antidepressants, etc.
  • Depakote = seizure med, antiepyleptic
43
Q

metabolic differential

A

hyperthyroid, b-12 deficiency (asterixis is the sign), hyperparathyroid, hypocalcemia, hyponatremia, renal dz, liver dz

44
Q

toxic differential

A

EtOH, Arsenic, caffeine, DDT, Lead Nicotine, Toluene, Withdrawal

45
Q

Huntington’s disease

A
  • Basal Ganglia Disease
  • Hereditary
  • CAG repeat disorder
  • Choreatic movements from excess excitation
  • Excess excitation!!
46
Q

HD pathophysiology

A
  • CAG Repeat disorder
  • Gene = “huntingtin” on Ch 4
  • Length of repeat correlated with age of onset – we don’t know why
  • Normal protein – axonal and vesicular transport, post-synaptic signaling, cellular survival
  • Mutant protein cleaved abnormally resulting in neuronal toxicity (Mitochondrial dysfunction, Altered transcription, Altered axonal transport, Altered calcium signaling)
47
Q

cerebral palsy

A
  • Not retardation!
  • Usually associated with hypoxic/traumatic delivery
  • Signs: definite hand preference < 1 yo; hypertonicity (UMN!); asymmetric crawling;
  • Upper motor neuron disorder!
48
Q

multiple sclerosis

A
  • Autoimmune likely
  • Destruction of myelin sheathing around central neurons
  • Hallmark – demyelinating episodes separated in space and time (In many cases there is recovery, There is a relapsing and remitting type, Separated in space = the plaques that show demyelination can jump around, the next time they have numbness, it could be in a different place)
49
Q

signs and symptoms of multiple sclerosis

A
  • sensory loss, muscle cramping/spasticity, loss of function (bowel, bladder, sexual); Optic neuritis, diplopia, HEAT INTOLERANCE, fatigue (Diplopia – two eyes don’t track together and look at the same things, SYMPTOMS GET WORSE IN HOT WEATHER!!! – Utaubs phenomenon)
  • Saltatory conduction – AP jumping from one gap junction to the other (The hotter you are, the faster ions are moving, the more leak there is out of the neuron, so the axon will be less efficient )

Physiology 2 (6 decks)

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