CN. Chapter 24 - 31 Flashcards
In what ways does the work of pediatric neuropsychologist differ form working with grownups?
1) The individual in question is growing. And this must be taken into perspective in assessment and rehabilitation.
2) Way more multidisciplinary. Working with both health, social services, education personnel and family members. (often these tasks involve explaining the child’s case to these groups. This may not only yield empathetic understanding of ‘oddities’ in the child’s behavior, but may also be useful in generating creative behavioral manegement solutions).
Is plastic reorganization more easily achieved in the younger ones (under 2 years)?
Not necessarily. Animal studies have shown some evidence, but it is not supported with research on human infants.
An important note about adjustment:
“Adjustment will be facilitated if the paediatric neuropsychologist does not describe the child’s deficits, but integrates findings into an explanation of the neurological disorder in the context of the child’s world and his or her past and future.”
What does PTA (often a good measure for severity of injury) stand for?
Posttraumatic amnesia.
There are several types of acquired brain injury. Can you give examples of different Hypoxic-ischaemic injury?
- Near drowning
- Anaesthetic accidents
- Prolonged status epilepticus
- Cerebrovascular accidents
Focal impairments to the frontal lobes in the teenage years generally lead to one of two behavioral phenotypes. Can you imagine what they might be?
1) irratability, anxiety, false euphoria, over sexualized behavior, poor social responses (My comment: So just executive function in general?)
2) Apathy, poor initiation, pseudo-depression.
Some epileptic syndromes are associated with specific cognitive sequelae. What are these?
- Moderate to severe learning difficulties are observed in majority of children with Lennox-Gastaut and West’s syndrome.
- Epilepsy is a co-symptom of severe learning diffeculities (9 - 31%), autism (11-35%) and cerebral palsy (18-35%).
- Intellectual decline in epilepsy (not associated with other underlying conditions) is usually associated with anti-epileptic drug (AED) toxicity.
What is Hydrocephalus?
In danish, also called: “vand i hovedet”. It is a secondary condition arising from a number of primary disorders. It is associated with:
- Gross and fine motor problems
- Greater impairment to language content than to structure
- List-learning problems
- Problems with focused attention
- Behavioral difficulties - children with shunted hydrocephalus have higher rates of behavior disorder, than those without.
(egen note: så alt er lort eller hvad?)
What characterizes ADHD (Attention deficit hyperactivity disorders)?
A triad of inattention, overactivity & impulsivity. Symptoms persist into adolescence in two out of three cases.
In what ways can ADHD be treated?
- Information provision
- Use of stimulant medication
- Family and school management advice
- Self-instructional training
What is especially important in diagnosing ADHD?
Diagnosis must be based on the persistence of symptoms across settings.
What is Specific learning difficulties?
The term is applied by educators to a number of ‘disorders’ (reading, writing, arithmetic and spelling) having some similarities in symptomatology to conditions seen in persons with an acquired brain injury. (p. 485)
What does NVLD stand for, and if you know, what is it?
Nonverbal learning disability (NVLD). Is a postulated condition of multiple aetiology including neuropathological disorders. It’s characteristics are:
- Bilateral tactile-perceptual difficulties particularly affecting the left side
- Impaired visual recognition and discrimination
- Problems with visuospatial organization
(As the name sort of suggest, auditory verbal processing is preserved. As are simple motor skills, selective and sustained attention for auditory-verbal information, reading and spelling.) (p. 486).
Glutamate is.. and mediates..?
An amino-acid. It mediates excitatory transmission in many central pathways. (Excessive release of glutamate may cause over-excitation of postsynaptic neurons)
GABA is.. and mediates..?
An amino-acid. It is the principal inhibitory amino-acid transmitter in supraspinal pathways. The inhibitory efferent pathways from the basal ganglia and the cerebellum are GABAergic and GABA also mediates inhibitory effects of intra-cortical neurons.
Acetylcholine is.. and mediates..?
Acetylcholine is the transmitter at skeletal neuromuscular junctions, parasympathetic effector junctions, and all autonomic ganglia. It mediates both excitatory and inhibitory effects in the central nervous system.
(Bonus: Cholinergic interneurons oppose the influence of dopamine in the basal ganglia, and manipulation of cholinergic function is an important strategy in the management of Parkinsons disease.)
Dopamine is.. and is synthesized from?
Dopamine is a catecholamine synthesized from the amino-acid tyrosine. Tyrosine hydroxylase converts tyrosine to L-DOPA, which is then converted to dopamine by aromatic amoni-acid decarboxylase.
The three principal dopaminergic pathways are?
- The nigrostriatal pathway (substantia nigra -> corpus striatum).
- The mesolimbic/mesocortical pathway (midbrain ventral tegmental area -> limbic structures and cerebral cortex).
- The tuberoinfundibular pathway (hypothalamus -> pituitary stalk)
Noradrenaline (norepinephrine) is.. and is synthesized from?
Noradrenaline is a catecholamine that is synthesized from tyrosine via the intermediate compounds L-DOPA and dopamine. The cell bodies of central noradrenergic neurons reside in nuclei in the pons and medulla.(Synaptically released noradrenaline is inactivated by re-uptake into terminals followed by re-storage or degradation by MAO).
Can you name three noradrenergic pathways?
- The dorsal noradrenergic bundle (coeruleocortical pathway: locus coeruleus -> neocortex and hippocampus)
- The ventral noradrenergic bundle (tegmental nuclei -> hypothalamus)
- Descending noradrenergic pathways (tegmental nuclei -> spinal cord and medullary autonomic nuclei)
5-Hydroxytrypyamine is also known as.. and is synthesized from? Where does the cell bodies of the neurons reside?
Serotonin, an indolamine synthesized from tryptophan via the intermediate precursor 5-hydroxytryptophan. Like noradrenaline, it is inactivated by by re-uptake into terminals followed by re-storage or degradation by MAO. Neurons reside in the raphe nuclei of the brainstem.
5HTergic (Serotonin) pathways include?
- Ascending pathways from the dorsal and (overlapping) median raphe nuclei.
- Descending raphe-spinal pathways.
Histamine is? and plays a role in?
Histamine is a monoamine. Histaminergic neurons are believed to play an important role in the maintenance of wakefulness and acid secretion in the stomach.
What are neuropeptides?
They are large molecules made up of sequences of amino-acids. One of the postulated roles of neuropeptides is to modulate the action of co-localized ‘classical’ transmitters.
There are two main receptor ‘superfamilies’, distinguished by the effector mechanism to which they are coupled. Can you name and describe them?
Ionotopic (ion-channel-coupled). receptors: The transmitter or drug, binds directly to the site on an ion channel, and thereby regulates the movement of ions in or out.
Metabotropic (G-protein-coupled) receptors: The binding of the drug or transmitter, initiates a cascade of events within the postsynaptic cell (fx. alterring the permeability of the membrane to particular ionic species)
What are agonists compared to antagonists?
Transmitters and drugs that stimulate receptors and evoke physiological responses are referred to as agonists. Antagonists evoke no response of their own but prevent the action of agonists.
What is meant by the sustained-release preparations?
That you can provide a patient with a gradual release of the drug from particles during their passage through the gut, thus allowing for example a once-daily dosis.
Speaking about drugs.. what is meant by the term ‘therapeutic range’ and ‘therapeutic index’ ?
The therapeutic range is the concentration range in which therapeutic effects are obtained without intolerable side-effects.
Therapeutic index is the ratio of the maximum tolerated concentration to the minimum effective concentration.
During continued use, tolerance may occur to the drug. This may arise from?
A change in tissue sensitivity (neuroadaptation, pharmacodynamic tolerance) and/or a change in the rate of elimination of the drug.
Can you name the two major classes of antidepressants?
Monoamine oxidase inhibitors (MAOIs)
&
Monoamine uptake inhibitors (fx. SSRI)
How does ‘MAOIs’ work?
MAOI’s block the enzyme MAO that normally destroys monoamine transmitters within presynaptic terminals. The increases the availability of the transmitter, and thus increases postsynaptic receptor stimulation. (MAOI’s are seldom the first choice of antidepressant due to their potential for adverse effects. Though sometimes used in some anxiety disorders).
How does monoamine uptake inhibitors work?
Re-uptake into presynaptic terminals is the principal inactivation machanism for monoamine transmitters. Uptake blokade, therefore potentiates monoaminergic transmission.
Monoamine uptake inhibitors can be classified into which categories?
Tricyclic antidepressants (TCAs), Selective serotonin re-uptake inhibitors (SSRIs), Selectictive noradrenaline re-uptake inhibitors (NARIs) and Serotonin-noradrenerline re-uptake inhibitors (SNRIs).
(SSRIs and more recently, NARIs and SNRIs, have become more popular because they have fewer side-effects and are safer in overdose than TCAs).
How well does SSRIs and NARIs and SNRIs work?
In double-blind trials, only about 40% of patients attain full remission of depressive symptoms. So it should be noted, that a favorable response to treatment is not the same as complete remission of symptoms.
Presentation of other antidepressant drugs than the more traditional, are described at page 506.
It really is.
How is Lithium administered and what does it do?
Lithium is administered as a salt. It has numerous effects on monoaminergic transmission, including facilitation of tryptophan uptake, increased 5-HT and noradrenaline release and prevention of postsynaptic dopamine receptor super-sensitivity.
The relationship between these effects and clinical mood stabilization is uncertain. (p. 506).
Which disorders can benefit from Lithium?
Mostly, manic-depressive illness (because of its mood stabilizing qualities perhaps). It is also sometimes used to help with management of impulsive agression.
How does Benzodiazepines work, and to who are they primarily administered?
Benzodiazepines bind to specific sites on the GABA(A) receptor-ionophore complex. GABA’s inhibitory action is mediated by the opening of CL- channels in postsynaptic membranes. Benzodiazepines potentiate (translation: “effectivises or risen”) GABA’s channel-opening action.
Benzodiazepines are effective in relieving the symptoms of generalized anxiety disorder (sometimes also in minor surgery, in alcohol withdrawal and as night time sedatives).
How does beta-adrenoceptor antagonists work and to what therapeutic use?
It blocks the effects of noradrenaline mediated by beta-adrenoceptors, including tachycardia (high heart rate) and tremor. Thus maybe breaking the vicious cycle: nervous -> heart beating -> more nervous -> even more heart beating -> even more nervous.
So, they are helpful in managing situational anxiety, fx. public speeches.
(I use heartbeat here because the drug does not help with sweating which is mediated by other stuff, but in my humble opinion is maybe worse, since it is visible to other people, and thus makes the person more nervous).
What is the main mode of action with Anti-epileptic drugs?
To suppress neuronal excitability, either by enhancing inhibitory neurotransmission or by suppressing excitatory transmission. Even though mono-therapy is preferred, it is often necessary with combination therapy when medicating for epilepsi.
(For a list of the about 12 different drugs, see p. 510).
Drug treatment of Parkinson disease aims to? And what drug is used?
- Restore dopaminergic function, or
- Restore the balance og dopaminergic/cholinergic function in the basal ganglia.
L-DOPA is the most effective treatment for PD. (Me: … And maybe deep brain stimulation?)
Can you descripe the side-effects to L-DOPA therapy?
Dyskinesias constitute a more serious problem for about 50% of patients during prolonged treatment. Behavioral side-effects include mood disturbances (depression or mania), insomnia, delirium and sometimes hypersexuality from limbic/hypothalamic dopaminergic hyperfunction.
What are the major neuropathological features of Alzheimer’s disease? And how can it be treated medically?
- Extracellualar plaques containing B-amyloid protein.
- Intraneuronal neurofibrillary tangles
- Neuronal loss
By using reversible competitive inhibitors of acetylcholinesterase ( Fx. Donepezil or Gallantamine)
What is meant by vascular disorders?
The term vascular disorders covers a range of conditions, including cerebrovascular disease (eg. stroke, vascular dementia) and specific blood vessel problems, such as aneurism and associated sub-arachnoid hemorrhage (SAH).
.. If one was to look at pre-stroke conditions, one might look into?
Hypertension (elevated blood pressure) or hypotension (Low blood pressure).
(A significant reduction in the probability of subsequent stroke or vascular dementia is achieved when hypertension has been successfully treated and blood pressure is reduced and controlled)
Describe what ‘Cerebral Small Vessel Disease (SVD)’ is?
It is a narrowing of penetrating arterioles which supply the deep white matter of the brain, leading to gradual ischemic damage. Diagnosis is confirmed by lesions in the white matter identified using MRI. (see p. 523 for more)
Try and describe what ‘Transient Ischaemic Attacks (TIAs)’ are.
TIAs are temporary (lasting less than 24 hours) neurological deficits arising from an ischemic episode, leading to a possible wide range of cognitive deficits. Early signs often include slowed speed of information processing and new learning.
What is a stroke? What is the neurological presentation?
A stroke is a disruption of vascular supply to the brain, of rapid onset with neurological symptoms persisting longer than 24 hours, caused by haemorrhage from an artery or from its occlusion through progressive narrowing of the vessel.
The neurological presentation can be extreme variable. When the stroke involves the language centers, aphasic problems often result. The ‘classic’ cognitive disturbance in right hemisphere stroke is perceptual deficit (i.e. left side of visual space does not exist).
What are the risk factors for Stroke?
Age, cardiac disease, smoking, prior TIAs (recall? Transient Ischaemic attacks), hypertension and diabetes.
What characterizes Vascular Dementia (VaD)? And how do diagnose it?
It is a generalised, significant reduction in cognitive function that is cerebrovascular in origin. (The term has replaced the older ‘multi-infarct’ dementia).
Diagnosis can be made, comparing the IQ figures obtained with the predicted pre-modbid IQ’s for the patient generated using NART (National adult reading test) and comparing these to WAIS-III scores.
What characterizes Subarachnoid Haemorrhage (SAH)? How do they most often arise?
The term ‘haemorrhagic stroke’ is usually applied to bleedings into the substance of the brain, whereas SAH refers to a blood vessel rupturing and bleeding into the subarachnoid space. About 80% of SAHs arise from the rupture of an aneurysm. (85% aneurysm are found on the anterior cerebral artery distribution. The next common are middle cerebral artery aneurysms, the posterier cerebral circulation having the lowest occurrence. This often cause some personality changes (i.e. the aneterior cerebral artery distribution)).
Lastly, SAH is more common in the younger population (50 - 55 years old) compared to stroke.
To read about different vascular surgeries, see p. 535.
535, yes.
