Anatomy, embriology: general Flashcards
WM tracts
cingulum
Cingulate gyrus to the entorhinal
cortex
Affect, visceromotor control;
response selection in skeletomotor
control; visuospatial processing
and memory access
X: Left-sided lesions cause verbal amnesia, whereas right-sided lesions alter visuospatial (location) memory; bilateral damage causes global amnesia.
Fornix
Hippocampus and the septal area to
hypothalamus
Part of the Papez circuit; critical in
formation of memory; damage or
disease resulting in anterograde
amnesia
Superior longitudinal
fasciculus
Frontotemporal and frontoparietal
regions
Integration of auditory and speech
nuclei
SLF + FA
Originally, the AF was first described as a component of the SLF, and their names were used as a synonym of each other. Recently, researchers have separated these bundles as the SLF and the AF that connect the frontal cortex to the occipital and parietal cortex, respectively (Dick & Tremblay, 2012; Gierhan, 2013; Petrides & Pandya, 2009). Damage to this tract can cause speech impairments such as anarthria and dysarthria
Inferior longitudinal
fasciculus
Ipsilateral temporal and occipital
lobes
The role of the ILF is therefore central in all activities involving processing complex visual information, from objects, faces, and word perception to emotion recognition and semantics (ffytche et al., 2010). Some of the behavioral and cognitive deficits described in patients with anterior temporal lobe damage are due to disconnection of the ILF fibers that prevent visual inputs to reach the limbic, paralimbic, and temporopolar cortex.
X: object recognition, visual agnosias, prosopagnosia
Cholinerg projection brain
Dopamine projection brain
GABA pathway brain
Noradrenergic projection of the brain
Serotonin pathway brain
Limbic system Papez circuit
Neuralation
Neurulation is a multistep process leading to the development of the central nervous system.
*
It starts at 21-day postfertilization in humans.
*
Neurulation is a process divided into primary neurulation and secondary neurulation.
*
Primary neurulation is a discontinuous process that starts at different points along the rostrum–caudal axis necessary for the neural tube closure.
*
The secondary neurulation permits the formation of the spinal cord at the lower sacral and caudal level.
Basal plate give rise to…
Periferial nerves
Axonal injury
Neurapraxia (“Nerve Dysfunctional”)
Neurapraxia Overview:
Nerve injury causing temporary interruption of action potential conduction without permanent damage.
Preservation of axon with no axonal degeneration.
Mild and reversible pathological changes.
Full and rapid recovery expected, typically within days to a few months.
Variability in Nerve Susceptibility:
Motor nerves are most susceptible to injury.
Pain and autonomic nerves are least susceptible.
Proprioception, light touch, and temperature modalities show intermediate susceptibility to injury.
Axonotmesis (“Axon Cut”)
Neurotmesis (“Nerve Cut”)
In neurotmesis, there is complete loss of axonal continuity. The cut ends of the nerve either remain separated, or they may reconnect through a bridge of scar tissue consisting of fibroblasts, Schwann cells, and regenerating axons. In any event, recovery is negligible. Hope for any functional recovery requires surgery
Axonotmesis regeneration
In axonotmesis, degeneration occurs distal to the injury
site, while the proximal segment exhibits few histologic or
pathologic changes. Distal segment degeneration is called
Wallerian degeneration, or anterograde degeneration, the
principal histologic change of which is a breakdown of both
axons and myelin, leaving only ghost-like endoneurial
sleeves. Schwann cells, and later macrophages, consume
the axonal and myelin debris. The complete process
unfolds over a period of weeks, ultimately reducing nerve
fibers to a mass of Schwann cells and endoneurial sheaths.
When the endoneurium is disrupted (Sunderland
type III) Wallerian degeneration proceeds (as described
above), with this difference: intrafascicular injury impairs
axonal regeneration. That is, damage to the endoneurium
causes shrinkage, fibrosis, and ultimately obliteration
of the endoneurial tubes, limiting axonal regeneration.
What is more, Wallerian degeneration is now accompanied by an additional pathologic process: degeneration of
the proximal segment in a retrograde direction.
Axonal and cell body degeneration
Degenerative changes in the cell body may include migration of the nucleus to the periphery of the cell and the
breakdown and dispersal of Nissl granules in a process
named chromatolysis. This process depresses cell body
protein synthesis. Regeneration of the cell body reverses
this process, reinstating protein synthesis, which in turn
facilitates axonal regeneration.
Lesion of cervical plexus
Plexus brachialis
Polio
Guillan Barré
Spinal nerve
GM in spine
Rexed Laminae
Hippocampal fibers
WM tracts and striatum
Thalamic fibers
Thalamus vascular supply
Cerebellar neurons and inputs
Types of cerebellar neurons and their inputs: mossy fiber pro-
jections from pontine n., vestibular n., red n., deep cerebellar n., spinal cord, reticular formation; climbing fiber projections from inferior olive.
Anterior mesenchephalis syndromes
Mid pons lesion
Lower pons lesions
Superior medulla
Inferior medullar lesion
Spinal trigeminal tract; medial lemniscus
Central herniation
Long tracts of spinal cord
reticulospinal tract
Course
Medial Reticulospinal Tract (Pontine): Descends ipsilaterally in the anterior funiculus [1] Responsible for controlling axial and extensor motor neurons e.g enable extension of the legs to maintain postural support ; Stimulation of the midbrain locomotor centre can result patterned movements (e.g. stepping)[3]
Lateral Reticulospinal tracts (Medullary): Descends bilaterally in the lateral funiculus [1] Responsible for flexor motor neurons [2]; Inhibits the medial reticulospinal tract and therefore extensor motor neurones enabling modulation of the stretch reflex [4]
Both the lateral and medial tracts act via interneurons shared with the corticospinal tract on proximal limb and axial muscle motor neurons.[1]
reticulospinal tract lesion
Pathology
Spastic paraplegia
Lesions to the cortico-reticulospinal system can result in decreased postural control and reduced selectivity of postural control.[3] If the excitatory fibres in the reticular formation have a leison this can result in hypotonia by the loss of descending excitatatory impulses to the spinal cord. Conversly in the inhibitory fibres are disrupted in the reticular formation this could result in hypertonia (spasticity) As the lateral reticulospinal’s is involved in inhibition, if this pathway is disrupted it can result in spasticity [4]. In addition due to the lack of descending inhibition, the medial reticulospinal tract would then maintain spasticity in the musculature.[4]
vestibulospinal tr
Upright Posture Maintenance: Performed by both the medial and the lateral vestibulospinal tracts. The medial tract supplies the muscles of the head and neck whereas the lateral tract supplies the muscles located in other parts of the body. When the head of the person moves, signals are sent by these vestibular tracts to specific antigravity muscles. These muscles contract and maintain the upright posture of the body.
Vestibulospinal Reflexes: A vestibulospinal reflex is the one that uses organs of the vestibular system and the skeletal muscles in order to maintain balance and posture[1]
vestibulo ocular reflex
Medial Vestibulospinal Tract
Vestibulo-ocular reflex lateroflexion of neck
Head and Eye Coordination: Performs the synchronization of the movement of the eyes with the movement of the head so that eyes do not lag behind when the head moves to one side. This function is very important for maintaining the balance of the body.
Head righting reflexes. These are responsible for keeping the head and gaze horizontal
Eye righting reflex (Vestibulo-ocular reflex) This origniates in the ascending medial longitudinal fasciulus and extends to the extraocular muscles of the eyes. The horizonal position of the eyes when the head is an upright postural set is caused by cancelling of the tonic acitiy of the deiteroocular pathways.[2] It is therefore able to keep the eyes still while the head moves, allowing images to focus on the retina [4]
Spinal grey matter somatotopy
vascular watershed zones of SC
Facial nerve components
bered 1 through 5) cause different neuro
-
logical symptoms because of the involved nerve components: 1
, facial weakness + impaired hearing + vestibular dysfunction; 2
, facial weakness + impaired taste sensa-
tion + decrease lacrimal & salivary secre-
tion; 3
, facial weakness + impaired taste sensation + decreased salivary secretion + hyperacusis; 4
, facial weakness + impaired taste sensation + decreased salivary secre-
tion; 5
, facial weakness. Greater petrosal nerve carries parasympathetics to the lac-
rimal and nasal glands. Stapedius nerve acts to dampen the tympanic membrane oscillation. Chorda tympani carries taste sensation from the anterior tongue
accessorius
Bladder disfunctions
retinal representation
CN III-VI
oculomotor nucleus
nystagmus types and patterns
less common nystagmus types
nystagmus types III
Bony jugular foramen