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140 Cards in this Set
- Front
- Back
when does the rostral neural tube close?
|
24 - 26 days
|
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when does the caudal neural tube close?
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26-28 days
|
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what is the result of failure of rostral neural tube to close?
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anencephaly
|
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what is the result of failure of caudal neural tube to close?
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spina bifida
|
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what structures are derived from the telencephalon?
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cerebral cortex
amygdala hippocampus striatum olfactory bulb |
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what structures are derived from the diencephalon?
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thalamus
hypothalamus epithalamus subthalamus retina |
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what structure is associated with the mesencephalon?
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midbrain
|
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which vesicle of the neural tube is associated with the pons and cerebellum?
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metencephalon
|
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what is the medulla derived from embryologically?
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myelencephalon
|
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what are the 3 vesicles of the neural tube in its 3 vesicle stage?
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prosencephalon
mesencephalon rhombencephalon |
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what is the dorsolateral signal involved in regionalisation of neural tube?
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bone morphogenic protein
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what is the ventral signal involved in regionalisation of the neural tube?
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sonic hedgehog
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are the oldest neurons located superficially or deep?
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superficially
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where is CSF found?
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ventricles
subarachnoid space |
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what is the volume of CSF?
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120-150ml
|
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how does CSF from the lateral ventricles drain into the 3rd ventricle?
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foramen of munro
|
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how do the 3rd and 4th ventricles communicate?
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aqueduct of sylvius
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how does CSF in the 4th ventricle drain into the subarachnoid space?
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foramina of Luschka (lateral) and Magendie (midline)
|
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what are the two layers of dura?
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periosteal layer
meningeal layer |
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what is the production rate of CSF?
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21ml/hour or 500ml/day
|
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what are the two sources of CSF production?
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choroid plexus
ependyma |
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what percentage of CSF production is choroidal?
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80%
|
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where are the majority of choroidal fissures?
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lateral ventricle (floor of body, temporal horns)
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t/f... the type (fast or slow) of neurotransmission is determined by the neurotransmitter
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false, it is determined by the postsynaptic receptor
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which of CSF and serum contains less protein?
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CSF
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which of CSF and serum have fewer chloride ions?
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serum
|
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where does CSF absorption mainly occur?
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arachnoid villi (venous sinuses)
|
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which transverse sinus is usually dominant?
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right
|
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t/f... CSF absorption is pressure dependent
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true
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t/f... CSF production is pressure independent
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true
|
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what is the effect of increased pressure on CSF absorption?
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absorption will increase
|
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what is the normal CSF pressure?
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7-15 cmCSF (5-12 mmHg)
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what are the four types of drug target protein?
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ion channels
receptors enzymes transport proteins |
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what are the four main types of receptors?
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ionotropic
G-protein coupled kinase linked nuclear |
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what type of receptor will result in fast neurotransmission?
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ionotropic receptors
|
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which type of receptor is associated with slow neurotransmission?
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G-protein coupled receptors
|
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at what level is a lumbar puncture performed?
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between 3rd and 4th lumbar vertebrae
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what is xanthochromia?
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yellow CSF (due to blood in CSF e.g. SAH)
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what is hydrocephalus?
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increased CSF volume
|
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what are the causes of congenital hydrocephalus?
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aqueduct stenosis
communicating myelomeningoceles |
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what are the causes of acquired hydrocephalus in newborns?
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intraventricular haemorrhage of prematurity
meningitis |
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what are the causes of hydrocephalus in adults?
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meningitis
haemorrhage tumour (blocking outflow of CSF) surgery aqueduct stenosis (LOVA) idiopathic |
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what are the cardinal signs of acute hydrocephalus?
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headache, nausea and vomiting followed by lethargy, drowsiness, stupor and coma
|
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what are the signs of acute hydrocephalus?
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papilloedema
diplopia setting sun sign false localising signs - 6th nerve palsy decreased level of consciousness |
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how does normal pressure hydrocephalus present?
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characteristic triad:
gait disturbance dementia urinary incontinence |
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which malformation is associated with myelomeningocele?
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Chiari II
|
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how does phenytoin work?
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limits the firing frequency of neurons
|
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how do barbiturates work in epilepsy?
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inhibit excitatory transmitter release
activating GABA receptors enhancing GABA action |
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how do benzos work in epilepsy?
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enhance GABA action
|
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how does carbamazepine work?
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lits firing frequency of neurons
enhances GABA action activates adenosine receptors |
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how does carbamazepine aggravate absence seizures?
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via potentiation of GABA(A) receptors possibly via a receptor subtype specific action in the ventrobasal thalamus
|
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how does sodium valproate work?
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inhibits GABA metabolism
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how does vigabatrin work?
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inhibits GABA metabolism
|
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how does tiagabine work?
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inhibits GABA uptake
|
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which drug mechanism has not yet been used in anticonvulsant therapy?
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excitatory amino acid antagonism
|
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how does lamotrigine work?
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inhibits glutamate release via effects on sodium channels
|
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what percentage of people with epilepsy do not have an identifiable cause?
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60-70%
|
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which epilepsy has the greatest risk for siblings?
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generalised (10%)
|
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what develops into the neural plate?
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ectoderm
|
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when does the neural groove develop?
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20 days
|
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when does the neural groove close to form the neural tube?
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by 22 days
|
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what percentage of the neurons formed in embryonic and foetal development do not survive?
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between 40 and 75%
|
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where are the serotonergic cells of the brainstem reticular formation?
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raphe nuclei
|
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which two neurotransmitter systems of the brainstem reticular formation are associated with ANS control?
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acetylcholine
noradrenaline |
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where are the dopaminergic cells of the brainstem reticular formation?
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substantia nigra
ventral tegmental area |
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where do the dopaminergic cells of the brainstem reticular formation project?
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forebrain
|
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what neurotransmitter is associated with the locus coeruleus?
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noradrenaline
|
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which tract might be affected if the patient has nystagmus?
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medial longitudinal tract
|
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what structures of the brainstem may be involved if a patient has dysphonia
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nucleus ambiguous
corticobulbar tract |
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what is the usual cause of vertigo, vomiting and nausea in brainstem lesions?
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vestibular nuclei
(or area prostrema) |
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what is the cardinal sign of a brainstem lesion?
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loss of pain & temp from contralateral body
loss of pain & temp from ipsilateral head |
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what is the sensory pattern of loss in a spinal cord lesion?
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loss of pain and temp contralaterally
loss of tactile ipsilaterally |
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which cranial nerves are associated with the nucleus of solitary tract?
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VII, IX, X
|
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which cranial nerves are associated with nucleus ambiguous?
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IX, X, XI
|
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what are the features of an upper motor neurone lesion to the facial nerve?
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contralateral lower facial muscle weakness
|
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what is the feature of a lower motor neurone lesion to the facial nerve?
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ipsilateral loss of upper and facial muscles
|
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which muscles of the face receive a contralateral input only?
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lower facial muscles
|
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which facial muscles have bilateral innervation?
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upper facial muscles
|
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when does the cranial neuropore close?
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day 24
|
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when does the caudal neuropore close?
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day 26
|
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what is anencephaly?
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failure of closure of anterior neuropore
|
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what forms from the telencephalon?
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cerebral hemispheres
|
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what forms from the diencephalon?
|
thalamus
hypothalamus epithalamus |
|
what forms from the mesencephalon?
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midbrain
|
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what forms from the metencephalon?
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pons and cerebellum
|
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what forms from the myelencephalon?
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medulla
|
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when is the brain neuronal proliferation complete?
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by about 16 weeks gestation
|
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where are the choroid plexuses located?
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ventricles
|
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what is the sulcus limitans?
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groove separating dorsal and ventral columns of the neural tube
|
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what is a myelomeningocele?
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midline bony defect over several lumbosacral vertebrae with a cystic structure containing meninges, nerve roots and dysplastic spinal cord tissue
|
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what is a meningocele?
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herniation of meninges through bony defect to form cystic lesion (does not contain nerve roots or spinal cord tissue)
|
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what event is responsible for spina bifida disorders?
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failure of closure of posterior neuropore in 4th week of gestation and subsequent failure of development of overlying skeletalmuscular and epithelial elements
|
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t/f... myelomeningoceles are produced by earlier defects than meningoceles
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true
|
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what percentage of spina bifida cystica are myelomeningoceles
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over 90%
|
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t/f... bladder and bowel involvement is almost always present in association with myelomeningoceles
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true
|
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what malformation is associated with myelomeningocele?
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Chiari II malformation
|
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what is hydrocephalus?
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increase in CSF in association with dilatation of ventricular system
|
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what is primary neurulation and when does it occur?
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elevation, folding and fusion of neural folds (completes early brain and spinal cord down to second sacral spinal level)
day19-26 |
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what is CSF?
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clear colourless ultrafiltrate of plasma with the same osmolarity but a slightly higher conc of Mg and Cl and slightly lower glucose and Ca
|
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how much CSF is found in lateral ventricles?
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25 ml
|
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how much CSF is in the III and IV ventricles?
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5ml
|
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how much CSF is in cranial subarachnoid space?
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25ml
|
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how much CSF is in spinal subarachnoid space?
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75ml
|
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what is the normal total volume of CSF?
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130ml
|
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what is the communication between the lateral ventricles and the IV vent?
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interventricular foramen
|
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how does CSF travel between III and IV vents?
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cerebral aqueduct
|
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how does the IV vent communicate with subarachnoid space?
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median aperture of Magendie
lateral apertures of Luschka |
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how much CSF is produced by the choroid plexus?
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80%
|
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what is the extra-choroidal production of CSF?
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capillaries of CNS (20% CSF production)
|
|
what is the formation rate of CSF?
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20ml/hour
|
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t/f... the rate of production of CSF is constant over a range of cerebral perfusion pressure associated with normal blood flow
|
true
|
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when will decreased CSF production occur?
|
sympathetic stimulation
ventriculitis acetazolamide |
|
how is CSF absorbed?
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by unidirectional valves (arachnoid villi) betwen subarachnoid space and blood located in venous sinuses of skull
|
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when does unidirectional flow between subarachnoid space and venous sinuses occur?
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when hydrostatic gradient between the two reaches 20-50 mmH2O
|
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t/f... CSF absorption is a passive process via pinocytosis
|
true
|
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t/f... the rate of CSF absorption is independent of pressure
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false, absorption is pressure dependent
|
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when do secondary sites of CSF absorption become important?
|
higher pressure
|
|
what are the mechanism of the development of an epileptic focus in the brain?
|
excess of neuronal excitation
deficiency of neuronal inhibition both |
|
how does phenytoin act?
|
limits firing frequency of nerve impulse conduction
|
|
which drugs reduce the neuronal release of glutamate?
|
phenobarbitone
carbamazepine |
|
which drugs enhance the activation of GABA-A receptors by GABA?
|
diazepam
barbiturates |
|
how does tiagabine work?
|
GABA uptake inhibitor
|
|
which drugs work by inhibiting metabolism of GABA?
|
sodium valproate
vigabatrin |
|
which antiepileptic drugs are frequently monitored?
|
phenytoin
carbamazepine sodium valproate |
|
which triad of side effects is associated with phenytoin?
|
ataxia
nystagmus gingival hyperplasia |
|
what do the neural crest cells eventuallly form?
|
peripheral nervous system - DRG, autonomic ganglia, adrenal chromaffin, melanocytes
|
|
what substances can cross the BBB?
|
low MW substances
lipid soluble substances |
|
what is the normal CSF pressure?
|
5-12 mmHg
|
|
what effect does pseudotumor cerebri have on CSF circulation?
|
increased CSF pressure
|
|
what are the symptoms of acute hydrocephalus?
|
headache
nausea/vomiting lethargy, drowsiness, stupor and coma |
|
what are the signs of acute hydrocephalus?
|
papilloedema, diplopia
setting sun sign false localising signs - th nerve signs decreased level of consciousness |
|
what is the characteristic triad of normal pressure hydrocephalus?
|
gait disturbance
dementia urinary incontinence |
|
what are the causes of normal pressure hydrocephalus?
|
idiopathic (elderly)
trauma SAH meningitis |
|
what is pseudotumor cerebri?
|
increased ICP in the absence of a mass lesion or hydrocephalus
|
|
who suffers from pseudotumor cerebri?
|
young overweight females
|
|
what is the prevalence of epilepsy?
|
1%
|
|
what percentage of people will have a seizure at least once?
|
5%
|
|
how does lamotrigine work?
|
inhibits glutamate release via effects on sodium channels
|
|
what is the diagnostic criteria for epilepsy?
|
2 or more seizures on more than one occasion
|
|
what are the causes of epilepsy?
|
birth injury
inborn error metabolism congenital malformation CNS infection head trauma stroke brain tumour |