Which NTs are considered catecholamines?
NE, DA, Epi
Anterograde transport in neurons carried out by (X). And retrograde transport by (Y).
X = kinesin Y = dynein
DA is (short/long)-range NT originating from which areas in brainstem?
Long;
Substantia nigra and VTA (ventral tegmental area)
List the three major distribution pathways of dopamine.
- Mesostriatal
- Mesolimbic
- Mesocortical
(X) dopaminergic pathway regulates movement via (exciting/inhibiting) (X) regions (caudate, putamen).
X = mesostriatal
Exciting
X = extra-pyramidal
(X) dopaminergic pathway regulates affect, reward, emotion by projecting to (Y).
X = mesolimbic
Y = Medial temporal lobe, cingulate cortex, amygdala
(X) dopaminergic pathway regulates cognition (working memory) by distributing to (Y).
X = mesocortical Y = neocortex (prefrontal cortex exclusively)
T/F: Dopamine synthesized from NE.
False - vice versa
(DA/NE/ACh/Glu) important in attention and maintaining wakefulness.
NE
T/F: Both DA and NE synthesized from Tryptophan.
False - from Tyrosine
SA is derived from Tryptophan
Raphe nuclei responsible for (X) neurons and are found in (lateral/midline) brainstem.
X = serotonergic
Midline
Rostral raphe nuclei project to (X) to control (Y).
X = forebrain Y = mood and emotion
Caudal raphe nuclei project to (X) to control (Y).
X = cerebellum, medulla, SC Y = pain perception
Histamine is found in (X) location in brain and projects to (Y).
X = hypothalamus (tuberomamillary nucleus) Y = forebrain, cerebellum, pons
(X) biogenic amine (NT) has important long-range projections to forebrain to maintain alert state.
X = His
Opioid-producing cells mainly found in (X) region(s) of brain/SC.
X = PAG and posterior horn of SC
Axons in periphery: collections of nerve fibers are bundled together in fascicles and surrounded by (X), composed of multiple layers of:
X = perineurium
Perineurial cells interconnected with tight junctions (blood-nerve barrier)
Which cells are allowed in the peripheral nerve fascicle? Star the most abundant of these.
- Schwann cells* (90%)
- Mast cells
- Fibroblasts
- Macrophages
List the connective tissue elements present in peripheral nerve fascicle.
- Basal (external) laminae around Schwann cells
2. Endoneurial fibers (collagen) - bind basal laminae together
T/F: Anterograde (Wallerian) degeneration causes axonal/terminal disintegration a few days post-injury.
False - within first 24 hours
List the morphological changes in cell body after axonal transection.
- Peripheral movement of nucleus
- Dissolution of Nissl bodies
- Stripping of synapse from dendrites/cell body
Peripheral neuron recovery from injury involves growth factors secreted by (X) that attract sprouting axons.
X = Schwann cells of new distal tube
Peripheral neuron recovery from injury: the tips of the neuritic sprouts LOVE (X).
X = laminin (major glycoprotien of external lamina)
Peripheral neuron recovery from injury: traumatic neuroma occurs if…
Sprouting axon (from proximal segment) can’t reach Schwann cell tubes (at distal segment)
Regeneration of central nerves is extremely rare due to lack of:
ECM (external lamina) to guide axon sprouts
Regeneration of central nerves is extremely rare due to presence of:
Central myelin (potent inhibitor of axonal growth)
(X) cells in CNS clear myelin (quicker/slower) than peripheral macrophages do, thus contributing to poor central nerve regeneration.
X = microglial
Slower
(X) cells in CNS wall off injured area, contributing to poor regeneration.
X = astrocytes
Consciousness, the components of which include (X) and (Y), depends on integrity of physio mechanisms that originate in which part of brain?
X = arousal Y = attention
Reticular formation (and other structures between hypothalamus and mid-pons)
Patient with Sx of indifference, abulia (low willpower), apathy likely has damage to (X) part of frontal lobe.
X = dorsolateral convexity and medial frontal lobes
Patient with Sx of disinhibition, irritability, lability, poor judgement likely has damage to (X) part of frontal lobe.
X = orbitofrontal area (ex: Phineas Gage)
Presence of inappropriate reflexes (grasp, rooting, glabellar, etc) in adult is referred to as (X) sign and reflects (focal/diffuse) cerebral disturbance.
X = frontal release
Diffuse (throughout frontal lobes)
Broca’s usually result of (X) affecting (Y) artery territory.
X = stroke Y = MCA
(X) aphasia may be accompanied by “pie in the sky” visual field cut.
X = Wernicke’s
T/F: Wernicke’s aphasia commonly a result of embolic stroke.
True
(X) aphasia characterized by prominent repetition deficit with relatively normal spontaneous speech/comprehension. Where is the lesion?
X = conduction
Arcuate fasciculus (white matter connecting Wernicke’s to Broca’s
(X) aphasia characterized by intact repetition with marked reduction in amount/complexity of spontaneous speech. Where is the lesion?
X = transcortical
Cortex surrounding Wernicke’s and/or Broca’s
Transcortical aphasia: reading comprehension (lost/preserved) and auditory comprehension (lost/preserved).
Both relatively preserved
T/F: Transcortical sensory aphasia is characterized by impaired auditory comprehension and preserved repetition.
True
Anomia is inability to (X).
X = generate names (common symptom in all forms of aphasia)
Alexia with agraphia is seen without aphasia when the lesion is located at:
Temporal-parietal region (esp angular gyrus)
Alexia without agraphia is seen when the lesion is located at:
L (dominant) visual cortex and splenium of CC
Alexia without agraphia: which visual defect is present?
R homonymous hemianopsia (entire R visual field blank)
Alexia without agraphia: patients can see words via (R/L) hemisphere, which reaches (R/L) visual cortex. So why can’t they read?
L; R
Can’t cross over (damaged CC splenium) to L cortex (needed to process language)
Korsakoff’s syndrome clinical features:
- Anterograde and “patchy” retrograde amnesia
2. Confabulation
T/F: EtOH toxicity directly causes Korsakoff’s.
False - vit B deficiency in alcoholics
Location of lesions seen in Korsakoff’s syndrome.
Diencephalon and frontal lobes (bilateral with atrophy of mammillary bodies)
Wernicke’s encephalopathy is associated with (X) deficiency and lesions in (Y).
X = thiamine (vit B1) Y = medial hypothalamus and mammillary bodies
Wernicke’s encephalopathy triad:
- Confusional state
- Oculomotor dysfxn
- Ataxia
What’s apraxia?
Inability to perform movement despite intact sensory and motor function
What’s agnosia?
Failure to recognize/ID stimulus
What’s astereognosis?
Failure of tactile recognition (associated with parietal lesions of contralateral hemisphere)
What’s prosopagnosia?
Inability to recognize faces (temporal or occipital lesions, usually bilaterally)