Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
53 Cards in this Set
- Front
- Back
Projections from which retinal photoreceptors will cross at the optic chiasm?
|
Those on the nasal side of the fovea centralis
|
|
T/F The macula lutea is medial to the optic disc
|
False
|
|
Name the course of projections from the retinal photoreceptors in the conscious image forming pathway
|
Retinal photoreceptor>
Optic nerve> Optic chiasm> Optic tract> LGN> Optic radiation> V1 |
|
What type of information is represented in one layer of the LGN?
|
Magno or parvocellular information from half a retina from one eye
|
|
Where is V1 located?
|
Banks of the calcarine sulcus
|
|
What are the functions and projections of the:
Suprachiasmatic nucleus Superior colliculus Pretectum Pulvinar |
SCh - projects to hypothal, on to pineal gland. Time keeper & melanin.
SC - attention and avoidance Pretectum - projects to Edinger-Westphal - pupillary reflex Pulvinar - projects to V2-V5 - attention and integration |
|
Which quadrant of visual field does the Meyer's loop contain?
|
Upper contralateral quadrant
|
|
Describe the process of visual signal transduction, from light hitting a rod or cone to a neural signal
|
Light hits photoreceptor>
Conform change and G protein cascade> Reduction in cGMP> Closure of Na and Ca channels> K channels remain open> Hyperpolarisation> Reduction in glutamate release |
|
What type of cell connects rods and cones to ganglion cells?
|
Bipolar cells
"Off" or "On" cell type determined by response to glutamate. "On Bipolar Cells" depol in response to glutamate, increasing activity in ganglion by inverting the hyperpolarised signal |
|
How are single points of the retina processed for different types of info (e.g. colour, shape, movement etc)?
|
Parallel Processing
Every point of retina is covered by every type of ganglion cell |
|
T/F peripheral vision is totally spared in macular degeneration
|
True
|
|
What is the ventral stream of the visual cortex concerned with processing? What would a lesion cause?
|
WHAT an object is
Difficulty with object processing |
|
What is the dorsal stream of the visual association cortex concerned with processing? What would a lesion cause?
|
WHERE and object is and how it is moving
Causes problems detecting motion and grasping objects |
|
T/F Cones in the retina connect to only one ganglion
|
SOMETIMES!!!
Cones in the central retina connect to only one ganglion, whilst cones in the periphery connect to many |
|
Damage to the temporal lobe is most likely to effect which part of the visual field?
|
The contralateral upper quadrant (in both eyes)
|
|
T/F Sympathetic activation causes pupil constriction mediated by sphincter pupillae
|
False
PARAsympathetic activation causes the following |
|
T/F Sympathetic activation causes pupil dilation mediated by dilator pupillae
|
True
|
|
What would the pupillary reflex be in someone with Relevant Afferent Pupillary Defect (RAPD)? What structure is most commonly affected?
|
Normal consensual response of effected eye, reduced direct response.
Optic nerve. |
|
Describe the facial symptoms and underlying pathology of Horner's Syndrome
|
Unilateral
Partial Ptosis (loss of symp innervation of superior tarsal muscle) Miosis (pupil constriction because of loss of symp inhib of sphincter pupillae) Anhidrosis (reduced symp causes reduced sweating) |
|
Which artery supplies the inner retina?
|
Central retinal artery (branch of opthalmic artery)
|
|
Which artery supplies the optic nerve?
|
Posterior ciliary artery (branch of opthalmic artery)
|
|
Giant cell arteritis of which artery is most likely to result in a pale retina and pale optic nerve? What other finding is commonly associated with these signs?
|
Opthalmic artery
Prominent temporal artery |
|
What is the predominant type of ganglion cell in the cochlea?
|
Type I (95%): large cell body, myelinated,
|
|
What is the primary factor determining whether hearing will be regained following a cochlear implant?
|
Age - must be young enough for neural plasticity
|
|
Describe the pathway of cochlear action potentials to the auditory cortex
|
Cochlea>
auditory n.> cochlear nucleus (open medulla)> superior olive (pons)> inferior colliculus (caudal midbrain)> medial geniculate body (thal.)> auditory cortex |
|
T/F Hearing sensed in one ear is processed bilaterally in the auditory cortex
|
True - the signal is split bilaterally from the cochlear nucleus
|
|
Which cell type forms myelin in the CNS?
|
oligodendrocyte
|
|
T/F Relapsing remitting is the major course/form of MS, representing around 60% of MS
|
False - ~80%
|
|
Name 5 signs associated with multiple sclerosis
|
optic neuritis
diplopia paraesthesia dysarthria and dysphagia limb weakness ataxia neurogenic bladder Uthoff's phenomenon (worse in heat) Lhermitte's sign ('electric shock' on neck flexion) |
|
What investigations should be done for a suspected case of multiple sclerosis?
|
Contrast MRI (lesions in GM)
Lumbar puncture for immunoglobulins |
|
T/F axons are spared from destruction due to demyelination in MS
|
False - although axonal loss is relatively much less significant than myelin
|
|
What is the cause of multiple sclerosis?
|
Probably a combination of genetic factors (30% concordance in MZT - MHCII?) and environmental (EBV??)
|
|
T/F prevalence of MS increases nearer the equator
|
False
The opposite is true, possibly due to protective nature of Vitamin D |
|
What is the mechanism of multiple sclerosis?
(n.b. AI mech is probable but evidence exists against) |
Environ + genetics>
Activated CD4+ in periphery> TH1 (>macrophage) TH2 (>Ab) CD8+ TH17 (leukocyte recruit) >> myelin damage |
|
How do T-cells penetrate the BBB in MS?
|
alpha-4 integrin binds endothelium
|
|
What therapies are used for multiple sclerosis?
|
Restore BBB with:
corticosteroids alpha-4 integrin antag (natulizimab) Reduce inflammation: interferron b (T cell prolif, MHCII, TNF prod) plasmapheresis |
|
What is the most common cause of neurologic disability in young adults?
|
Multiple sclerosis
|
|
What are typical signs of multiple sclerosis at ONSET?
|
weakness, diplopia, optic neuritis, unsteady gait, vertigo, sphincter disturbance
|
|
Name five signs in ESTABLISHED multiple sclerosis?
|
Motor: UMN weakness, spacticity, Uthoff's
Sensory: parasthesiae, numb, pain, Lhermitte's, trigeminal neuralgia Cerebellar: gait ataxia, intention tremor, dysarthria Opthal: optic neuritis, diplopia, polydirectional nystagmus Sphincter disturb: urge incontinence, frequency |
|
T/F Th1 cells are probably more important than Th2 in the pathogenesis of multiple sclerosis
|
True
Lymphocytes are often absent in early MS lesions |
|
How is a diagnosis of multiple sclerosis made?
|
1. Clinical signs and symptoms
2. Imaging: lesions in CC, periventricular, brainstem, cerebell, SC 3. CSF: protein elevation (in ~30%), increased IgG in oligoclonal bands (in ~75%) |
|
Which correlates better with loss of function in multiple sclerosis: axonal loss or myelin loss?
|
axonal loss
|
|
List in order of smallest > largest (structure wrapped)
Endoneurium Epineurium Perineurium |
Endoneurium (surrounds axon)
Perineurium (envelopes fascicle) Epineurium (binds fascicles) |
|
Name the process that describes the degeneration of a nerve distal to a cut/crush point
|
Wallerian degeneration
|
|
Define a motor unit
|
A single motor neuron plus the fibres it innervates
|
|
Describe the cross-sectional appearance of a group of muscle fibres that have lost an innervating axon
|
Loss of chequerboard appearance. Previously multiple fibre types are replaced by a single fibre type of the neighbouring axon that reinnervates.
|
|
Describe the pathophysiology and primary fibre type effected by beri beri
|
Thiamine deficiency (B1) causes loss of small and distal fibres. Can be caused by alcoholism. Predominantly sensory rather than motor.
|
|
Describe the peripheral neuropathy caused by pernicious anaemia
|
B12 deficiency (stores last 10 years)
Demyelinating and axonal loss May be autoimmune |
|
Describe the peripheral neuropathy caused by Charcot-Marie-Tooth
|
An inherited, length-dependent dysmyelination causing foot-drop, clawed toe, high arched foot and lower leg wasting
|
|
Describe the peripheral neuropathy caused by Guilla- Barre syndrome
|
An acute inflammatory demyelinating (autoimmune) response to Schwann cells. Causes acute motor weakness/paralysis and hypo/areflexia. Often resolves spontaneously.
|
|
What proportion of diabetics experience a related neuropathy?
|
~30%
|
|
Describe the character of neuronal loss in diabetic neuropathy
|
Focal, peripheral and autonomic
|
|
Describe the pathophysiology behind diabetic neuropathy and how to prevent it
|
Neurons are obligate glucose users
High blood glucose> High neuronal sugar> Disrupted energy transfer in mitochondria, increased ROS, peroxidation of lipids and protein> Neuronal death + impaired glial metabolism and endoneurial ischaemia Prevention: tight control of blood sugar |