Neuro Block 3-Pt 1

ptheodore's version from 2016-07-22 15:20

Basal Ganglia

Question Answer
Which neurotransmitter is is depleted in Parkinson's DiseaseDopamine
Rigidity; slowness; resting tremor; mask-like facies; shuffling gait, associated with degeneration in the basal ganglia and substantia nigra .Parkinsonism
Sudden jerky and purposeless movements (e.g. Sydenham's chorea found in rheumatic fever; Huntington's chorea, an inherited disorder).Chorea
Slow writhing, snake-like movements, especially of the fingers and wrists.Athetosis
A sudden wild flail-like movement of one the limbs.Hemiballismus
Globus pallidus + PutamenLentiform nucleus
Lentiform + CaudateCorpus striatum
Caudate + PutamenNeostriatum (striatum)
Cortex to striatum (caudate and putamen)Corticostriatal (Afferent pathways (towards striatum))
Amygdala to ventromedial caudate and putamen (suggests that BG may have limbic and non-limbic components).Amygdalostriatal (Afferent pathways (towards striatum))
SNpc to various BG structures (and others).Nigrostriatal (Afferent pathways (towards striatum))
From centromedian (and other) thalamic nuclei to striatum (caudate and putamen).Thalamostriatal (Afferent pathways (towards striatum))
From striatum (caudate and putamen) to globus pallidus.Striatopallidal (Efferent pathways(from striatum to somewhere else))
From striatum (caudate and putamen) to substantia nigra.Striatonigral (Efferent pathways(from striatum to somewhere else))
Globus pallidus to thalamus.Ansa lenticularis (Efferent pathways(from striatum to somewhere else))
Globus pallidus to subthalamus.Fasciculus lenticularis (Efferent pathways(from striatum to somewhere else))
Blood supply to The head of the caudateAnterior cerebral & the recurrent artery of Heubner
Blood supply to internal capsuleAnterior Choroidal Artery
Movement disordersDyskinesia
Involuntary spontaneous movements.Hyperkinesia
Lack of spontaneous movement, and slowing of voluntary movement.Hypokinesia
A series of rapid, jerky, involuntary movements.Chorea
Continual uncontrolled writhing movements (disappear during sleep).Athetosis
Choreiform movements may eventually slow down and become athetosis movements; this is calledChoreoathetosis
A severe form of athetosis. Extreme contraction of antagonist muscle groups results in limbs locked in one position for long periods of time. Also may go in and out of muscle spasms.Dystonia
Involuntary flinging of limbs.Ballismus
Results from loss of enkephalinergic neurons in the striatum (Indirect Pathway).Huntington’s Disease
Dementia sometimes precedes the development of involuntary motor movements. Choreiform movements are the main symptoms. Degeneration of caudate nucleus and subsequent enlargement of ventricles.Huntington’s Disease
Stroke-induced, results in involuntary flinging of contralateral limbs. Damage to STNBallismus (or Hemiballismus)
Usually follows viral infection, particularly acute rheumatic fever (ARF) or Group A beta-haemolytic Streptococcus; that destroys cells in the corpus striatum of the basal ganglia.Sydenham’s Chorea
Symptoms: ‘Milkmaid’s grasp’, choreic movements, darting tongue, pronator sign (ask them to put their hands over their head, and it pronates out), and behavioral or cognitive changes.Sydenham’s Chorea
Bradykinesia: Poverty and slowness of movement. Tremor: Only seen while extremity is at rest; disappears during sleep. Rigidity: Resistance to passive limb movements. (Lead pipe rigidity). Tremor and rigidity is called Cogwheel rigidity.Parkinson’s Disease
Loss of neuromelanin (as substantia nigra cells die), Lewy bodies proliferate.Parkinson’s Disease
Is the most debilitating aspect of Parkinson’s Disease. It is a true slowing of movement.Bradykinesia
Was a designer drug (a bad one) that went straight to the substantia nigra and killed everything. The resulting effect was a profound Parkinsonism in these individuals.MPTP
Treatment for Parkinson’s Disease. _____is the precursor to dopamine. It is administered systemically and is converted to dopamine in the brain.L-Dopa
Sinemet is an L-Dopa/Carbidopa combination. Carpidopa decreases degradation of L-Dopa in systemic circulation, resulting in less side effects.Treatment for Parkinson’s Disease
Lesioning ‘non-essential’ portions of these structures. A relatively common procedure in the 50’s and 60’s prior to L-Dopa therapy.Pallidotomy and Thalidotomy
Bilateral electrodes (DBS) targeted at this structure is Effective in reducing tremor (resting and essential tremor) in Parkinson’s Disease.Thalamus
Bilateral electrodes (DBS) targeted at this structure is Potentially very effective in reducing tremor and most other Parkinson’s Disease symptoms.Subthalamus
Bilateral electrodes (DBS) targeted at this structure may reduce drug-induced side effects in patients who have already received pallidotomy for Parkinson’s Disease.Globus pallidus
Wobbling of head of body, when not doing anythingTitubation
Is commonly described as an action tremor (it intensifies when one tries to use the affected muscles) or postural tremor (present with sustained muscle tone) rather than a resting tremor, such as is seen in Parkinson’s, which is usually not included among its symptomsEssential tremor
Is a syndrome of sustained muscle contractions, frequently causing twisting and repetitive movements, or abnormal postures.Dystonia
Thought to occur following lesions of the lentiform nucleus.Dystonia
L-Dopa, anticholinergics, anti-spasmodics, Botulinum toxin, analgesics, etc). Surgery, (pallidotomy, thalidotomy, DBS), for severe cases. These can be used to treatDystonia
Characterized by multiple motor tics and at least one verbal ticTourette’s Syndrome
Copper accumulation in various basal ganglia structures, mostly the lentiform nuclei. Slit Lamp used to diagnoseWilson’s Disease
Copper accumulation in the liver (enzyme deficiency) results in chronic fatigue, hepatitis, cirrhosis. Copper is also released by the liver into blood (not bound to ceruloplasmin) and deposits in eyes (Kayser-Fleischer rings), kidneys and brain.Wilson’s Disease

Basal Ganglia Clinical Summary

Question Answer
Lesion to Globus pallidus results inTourette’s Syndrome
Lesion to Striatum/neostriatum results inHuntington’s
Lesion to Subthalamic nucleus results inBallismus
Lesion to Substantia nigra results inParkinson’s Disease
Lesion to Various structures of results inWilson’s Disease
Lesion to; Damage during pregnancy results inCerebral palsy
Thought to occur following lesions of the lentiform nucleus.Dystonia
Copper accumulation in various basal ganglia structures, mostly the lentiform nuclei. Slit Lamp used to diagnoseWilson's Disease

Cerebral Cortex


Question Answer
At the posterior pole of the eye, contains only cones, has few or no blood vessels, point of greatest visual acuity,only layer of cones presentFovea centralis of the macula lutea
The optic nerve is composed of axons arising from which of the following cells of the retina?Ganglion Cells
Extraocular muscles are attached to theSclera
Clear extension of the scleraCornea
Layer underneath sclera containing blood vessels.Choroid (vascular layer)
Part o the choroid, determines shape of lens and produces aqueous humor (Ant. Chamber).Ciliary Body
Absorbs scattered light.Choroid
Adjustable diaphragm that surrounds the pupil. Constrictor and Dilator muscles attached to it.Iris
Innermost layer of the eye that contains rods and cones.Retina
Center of retina. Contains the Fovea Centralis.Macula
CN II, veins, arteries, exit the eye here.Optic Disc
Depression in the center of the Optic Disc.Optic or Physiological Cup
Watery fluid in the front section of the eye (Anterior Chamber).Aqueous Humor
Jelly-like fluid in the back part of the eye. Produced by cells in the non-pigmented portion of the ciliary body.Vitreous Humor
Peripheral and B&W vision. 120 million.Rods
Color and central vision. 6 million.Cones
What kind of cells form the optic nerve.Ganglion cells
Between choroid and retina. Pigment epithelium
Provides blood-brain barrier for eye, degeneration of this structure is involved in macular degeneration and retinitis pigmentosa (Affects Peripheral) visionPigment epithelium
Drainage of aqueous humor is blocked resulting in increased intraocular pressureGlaucoma
Clouding of the lens. Causes include diabetes, aging, excessive steroid use, smoking, too much sun.Cataracts
Leading cause of blindness age 75 and over. Progressive loss of visual acuity, color vision, etc.Macular degeneration.
A non-inflammatory congestion of the optic disc (papilla) due to increased intracranial pressure.Papilledema
Hereditary condition causing progressive deterioration of rods, resulting in loss of peripheral vision.Retinitis Pigmentosa
Blood vessels swell, proliferate and distort. Will cause blindness if untreated. Laser surgery is the most effective treatmentDiabetic Retinopathy
Upper Visual Field Lower Bank of Calcarine Sulcus (Lingual Gyrus)
Lower Visual FieldUpper Bank of Calcarine Sulcus (Cuneus Gyrus)
Visual Cortex receives fibers fromLateral Geniculate Nucleus
Layers 2,3, & 5 of the lateral geniculate nucleusNasal Fields
Layers 1, 4 & 6 of the lateral geniculate nucleusTemporal Fields
Layers 1 & 2 of the lateral geniculate nucleusMagnocellular pathway
Layers 3,4,5 & 6 of the lateral geniculate nucleusParvocellular pathway
Fibers from the lateral geniculate nucleus project to what layer of the visual cortex4th layer
Small neuron cells in the LGN which receive input from small ganglion cells in the retina.Parvocellular Neurons
Large neuron cells, receiving input from large ganglion cellsMagnocellular Neurons
One and a Half Syndrome occurs at the level of thePons
Frontal eye field projects toContralateral pons (PPRF, CN VI)
Damage here results in decreased eye movements towards the opposite side (i.e. left side damage, decreased eye movements towards right), and neglect.Parietal lobe lesions (Parietal eye field is superior parietal lobule)
Plays a big role in reflexive eye movements, but damage here results in minimal symptoms because of so many different connections (i.e. area 8 also talks to PPRF, etc.).Superior Colliculus
Superficial layer of Superior ColliculusReceives info from retina and visual association areas (18, 19).
Middle layer of superior Colliculus receivesFrontal eye field info.
Deep layer of Superior ColliculusGets ascending sensory info.
Light stimulates the afferent component of CN II; these axons synapse in bothPretectal areas
Neurons in the pretectal areas send axons to theEdinger-Westphal nucleus of CN III (bilaterally).
Efferents from CN III innervate the pupillary sphincter via the _____, causing pupillary constriction.Ciliary Ganglion
Characterized by an absence of direct and consensual light reflexes (pupillary response). Miotic reaction to accommodation/convergence is still intact. May result from syphilis, diabetes, and lupus.Argyl Robertson Pupil
Blind spots in the visual fields.Scotoma
Asymmetric pupils. Important to note this can be present in ‘normal’ people.Aniscoria
Relative Afferent Pupillary Defect, A.K.AMarcus Gunn pupil

Visual Pathway Lesions & Blood Supply

Question Answer
Unilateral blindness. Trauma, optic neuritis.Lesion of the Optic Nerve
Binasal hemianopia.Lesions outside of Optic Chiasm
An internal carotid aneurysm could cause aUninasal hemianopia.
Calcified internal carotid arteries could causeBinasal hemianopia
Bitemporal hemianopia.Middle of Optic Chiasm, Pituitary tumor or craniopharyngioma.
Right/left homonymous hemianopia.Optic Tract
Meyer’s loop or lower part of the geniculocalcarine tractUpper quandrantinopia.
Lesion of Upper part of geniculocalcarine tractLower quandrantinopia.
Homonymous hemianopia typically with macular sparing.Visual cortex
Macular sparing may occur because of anastomosis of the ______ & _______ in the most posterior region of the visual cortex, which receives macular fibers. Calcarine & Middle Cerebral arteries
Bilateral damage of lingual gyrus (Area 17).Upper altitudinal hemianopia,
Bilateral damage of cuneus gyrus (Area 17)Lower altitudinal hemianopia
Blood supply to the Optic Nerve Basically the circle of Willis
Blood supply to the Chiasm Anterior cerebral, internal carotid
Blood supply to the optic tracts Posterior communicating, anterior choroidal
Blood supply to the LGNPosterior cerebral, anterior choroidal
Blood supply to the Geniculocalcarine tract (from LGN to visual cortex)Middle cerebral, anterior choroidal, and calcarine
Blood supply to the Visual cortex Calcarine + MCA
Calcarine artery is a branch of thePosterior Cerebral artery
Anterior choroidal branches come off theInternal Carotid arteries
Superior and inferior rectus move the eye whenAbducted
Superior and inferior oblique move the eye whenAdducted.
Lesions of CN III, IV or VI are at what level?Nuclear level
Lesions of the MLF are at what levelInternuclear level
Horizontal gaze; Frontal eye fields (area 8) damage is at what levelSupranuclear level
Vertical gaze; Pontine tegmentum (pons and midbrain). damage is at theSupranuclear level
Ptosis, mydriasis, diplopia. Eye is ‘down and out’CN 3 damage
Strabismus: misalignment of the eyes ‘at rest’ or during ‘relaxed forward gaze’.CN 3 damage
Lack of abduction, medial deviation at rest (strabismus). Horizontal diplopia only, when looking in direction of lesion.Damage to CN VI / Lateral Rectus Muscle
Patient will tilt head forward to compensate for problems with elevating the eye. This is vertical diplopia (dejected appearance). Head tilt is towards a nucleus, and away from a nerve, lesion. Or stated differently, head tilt is always away from affected eye.CN IV lesion
Destruction of ______ results in conjugate deviation of the eyes towards the lesioned side, and inability of the eyes to look voluntarily to the opposite side.Frontal eye field

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