Wednesday, April 12, 2017
Tuesday, April 11, 2017
Thalamus.
let's quickly learn a few basics and beyond in today's post on Thalamus.
1) Specific Sensory Nuclei
2) Association Nuclei
3) Nonspecific Nuclei
4) Motor Nuclei.
Specific Sensory Nuclei :These receive all sensory afferents. The arrangement of fibres is topographic and so is their projection to the somatosensory cortex.
The thalamic nuclei activate some thalamic interneurons as well as an area in the sensory cortex. Activated sensory cortex also sends impulses back to the thalamic relay nucleus, thereby modulating the thalamic output.
These help achieve integration of different types of sensory information.
These also receive sensory information but project to the cortex in a diffuse manner. Therefore they seem to be involved in the arousal induced by sensory stimuli.
They also project to the limbic system, thereby suggesting their involvement in the emotional impact of sensory stimuli.
They relay and process messages from the basal ganglia and cerebellum to the motor and premotor cortex.
2) Hypotonia, muscular weakness and incoordination,
3) Volatile emotions, pleasant or unpleasant.
-Medha.
Monday, April 10, 2017
Treatment of migraine headaches mnemonic
Hello! Here's a short post on treatment of migraines!
Treatment of acute migraine attacks mnemonic: NSAiDs
N: NSAIDS like Naproxen, S, Aspirin, Ibuprofen, Diclofenac
S: Sumatriptan (And other Triptans such as rizatriptan, eletriptan, almotriptan, zolmitriptan, naratriptan, and frovatriptan)
AiDs: Antiemetic/dopamine receptor antagonists: Chlorpromazine, prochlorperazine, and metoclopramide
Ds: Dihydroergotamine and ergot derivatives
Prophylaxis of migraine mnemonic: ABC
Antidepressants: Amitriptyline and venlafaxine
Beta blockers: Metoprolol, propranolol, and timolol
AntiConvulsants: Valproate and topiramate
Calcium channel blockers (less effective): Verapamil, Flunarizine
That's all!
-IkaN
Why do we feel sleepy when we are sick?
Hellooo Everybody,
Let's delve into some sleep physiology and learn about some sleep producing substances breifly!
The chemical agents which might be responsible for induction of sleep have been obtained from experiments on sleep-deprived animals.
The first experiments of this type were performed by Henri Pieron in 1913 on dogs. He demonstrated that dogs receiving CSF from sleep-deprived donor dogs slept for hours, while the recipients of CSF from normal donors remained awake. Recent work has confirmed these observations and identified several candidate sleep producing substances (SPS)
Sleep-deprivation presumably leads to a rise in the production of these substances in the brain tissue, cerebrospinal fluid,and even urine, through a negative feedback effect.
The best known SPS :
1) Muramyl dipeptide (MDP)
2) Delta sleep-inducing peptide (DSIP)
3) Arginine vasotocin (AVT)
4) Interleukin-1 (IL-1).
Besides these, there are about 20 more putative sleep-inducing factors.
Most of the known sleep producing substances induce Slow Wave Sleep.
After learning the physiology let's answer our question:
Muramyl dipeptide (MDP) is a component of bacterial cell( which acts via IL-1.) walls ,whereas IL-1 is released in infections.
IL-1 potentiates GABA-induced increase in permeability to chloride at synapses causing inhibitory effect on the Brain.
Nitric oxide may be part of a second messenger system which mediates the effect of IL-1 on sleep.
Lastly, IL-1 induces release of growth hormone releasing hormone (GHRH) which in turn releases growth hormone. Growth hormone itself enhances REM sleep and inhibits Slow wave sleep.
This explains why we feel sleepy when sick!
IL-1 also induces fever, and is therefore also called endogenous pyrogen. Antipyretics, such as aspirin, suppress the fever induced by IL-1 but do not affect the sleep-inducing effect of IL-1.
Like fever, sleep is a smart response which perhaps helps recovery by compelling the patient to take rest.
Isn't it truly remarkable, how our bodies work!
Let's Learn Together!
-Medha.
Brain Function Imaging.
Hello everybody!
Today we shall breifly learn as to how we can study the brain function using imaging techniques.
Positron Emission Tomography (PET)made debut in 1980s; two more imaging techniques came in the 1990s: functional magnetic resonance imaging (fMRI) and magnetoencepalography (MEG).
1) Positron Emission Tomography:
This technique makes it possible to see in an image which part of the brain is active during a particular task.
As we also know that although brain as a whole does not consume significantally more energy when it is active than when it is idle, metabolic activity does increase in circumscribed regions of the brain when these regions are functionally active.
This increased metabolic activity in the brain is the basis of PET.
In this technique a positron-emitting isotope is tagged to a molecule of biological interest such as glucose or a neurotransmitter.
For example, the positron-emitting isotope of fluorine (18F) is tagged to deoxyglucose and it is injected intravenously.
Deoxyglucose is taken up by neurons in the same way as glucose, but it can neither be fully metabolised nor can it come out of the neurons.
Since functionally active neurons take up more glucose, active regions of the brain accumulate more deoxyglucose.
So , following visual stimulation, 18F-deoxyglucose accumulation can be seen in the visual cortex. This signifies increased glucose metabolism in the visual cortex. Thus we have evidence for involvement of specific regions of the brain in specific functions
Positron emission is detected by appropriate detectors which construct a series of computerised images of the brain similar to those seen in computerised tomography (CT).
2) Functional MRI :
It is based on the principle that increased neuronal activity leads to a local increase in blood flow through the active part of the brain.
The increase in blood flow is somewhat greater than is warranted by the increase in oxygen consumption.
Therefore, blood flowing through the active, hyperemic region of the brain has more oxygenated haemoglobin than the blood flowing through less active regions of the brain.
The magnetic properties of oxygenated and deoxygenated haemoglobin are different, the magnetic resonance signals from the active region of the brain increase.
Functional MRI systems currently in common use give a spatial resolution of about 1 mm, but a resolution of 0.5 mm has been achieved in experimental settings. This is an important breakthrough because cortical columns also have a width of about 0.5 mm.
3)Magnetoencephalography (MEG):
It can complement the information obtained from the conventional electroencephalography (EEG). MEG is based on the principle that neuronal activity in the cerebral cortex generates not only fluctuations in electrical potential (detected by EEG) but also magnetic fields. Unlike EEG signals, MEG signals are not distorted by the intervening tissues. These technical advances have given hope for rapid progress in localization of functions in the human brain.
So I hope ,this helps you guys to have a better picture on Brain Imaging.
Let's Learn Together!
-Medha.
Absolute contraindications for trial of labor
Here are a few conditions in which trial of labor is absolutely contraindicated:
1. Classical cesarean section. (Vertical incision)
2. Abdominal myomectomy with uterine cavity entry.
Previous cephalopelvic disproportion is not an absolute contraindication for trial of labor (Because if the fetus is small in this pregnancy, a trial of labor can be done.)
Previous low transverse cesarean section (Horizontal incision) is not a contradiction for trial of labor.
These are the ones I found out about. Lemme know if there are more, we'll add them to the list!
That's all!
-IkaN
Sunday, April 9, 2017
Toxic Ventral Horn Cell disease
Hey guys!
The only ventral horn cell disease famous in India is Polio which was successfully eradicated. During it's era, other diseases with similar clinical picture, such as Kugelberg-Welander syndrome, Cerebral palsy, Friedreich's Ataxia, Spina Bifida etc were rampantly misdiagnosed as Polio.
Hence after it's eradication the incidence of these rare disorders has increased!
The disease is also known as "Infantile paralysis" and this moniker can't be more inaccurate. The commonest manifestation of this disease is Aseptic meningitis presenting with headache, photophobia, etc. And only 1% cases develop into paralytic poliomyelitis. And another point is that adults are 15 times more likely to become paralysed and are more likely to die.
Sorry for going off topic above; couldn't help it. Fortunately there are no drugs that are known to cause ventral horn cell disease. But there is one chemical called- TriocP, full form is tri-ortho-cresyl phosphate. It is illicitly used as a component of country liquor especially in USA; and in Mediterranean countries it was used as an adulterant in cooking oil.
Another toxic cause is Tick paralysis. The ixodes tick secretes a toxin that can cause Ataxia, flaccid asending paralysis, bulbar palsy etc closely mimicking Guillian barre's syndrome.
That's all!
-VM
Saturday, April 8, 2017
Lasegue's Test
Hey guys here's another clinical sign!
Lasegue’s sign is another name for the modified straight leg maneuver used in the diagnosis of lumbosacral radiculopathy.
To perform the straight leg test, the clinician lifts the extended leg of a patient in a supine position. A positive response occurs when the pain pattern of the lumbar radiculopathy is reproduced. The test should be stopped when the pain is reproduced or maximum flexion is achieved.
But this sign is difficult to evaluate clinically especially for students. The reason being as simple as that it has been performed many a times before and patient already knows that he is going to suffer pain. So it was modified a bit by Lasague, he proposed that the leg should be raised while the knee is flexed by flexing the thigh at the hip joint. And then the knee is slowly extended until the patient complains of pain. In severe cases patient will complain of pain even during the flexion of hip.
More useful than the straight leg maneuver is the crossed straight leg test. This test has a lower sensitivity but a higher specificity. The crossed straight leg maneuver is performed by raising the unaffected leg in a similar manner to the straight leg test. The examiner looks for the reproduction of radicular pain with elevation of the opposite leg.
A supplement to this straight leg raising test is Braggard's test. First we have to start raising the leg of the patient while his knee is extended until he complains of pain and then dorsiflex his foot, if the pain worsens, it's a positive Braggard's test.
But as given in most books, these signs are not only positive in case of lower lumbar vertebral disc lesions but also in a no of other conditions. The differential diagnosis of a positive straight leg test includes:
1. disc protrusion with impingement of nerve roots below L4;
2. meningismus;
3. any intraspinal lesion such as tumor below L4;
4. malignant disease or
5. osteomyelitis of the ilium or upper femur;
6. ankylosing spondylitis;
7. fractured sacrum and more.
That's all!
-VM
Tinel's Test
Heyy guys!!
Tinel's sign is the sign that a nerve is irritated. Tinel's sign is positive when lightly banging or percussing over the nerve elicits a sensation of tingling, or 'pins and needles,' in the distribution of the nerve.
For example, in carpal tunnel syndrome, where the median nerve is compressed at the wrist, the test for Tinel's sign is often positive, eliciting tingling in the thumb, index, and middle fingers.
Procedure: First you have to hyperextend the wrist to get the median nerve in the carpal tunnel more juxtaposed to the flexor retinaculum. Then tap the skin over the flexor retinaculum midway between pisciform bone and hook of hamate and then observe the patient's response.
This test can also be useful in the diagnosis of Tarsal tunnel syndrome where the tibial nerve is entrapped.
Another test in Carpal tunnel syndrome is Phallen's test.
-VM
Pathophysiology of atrophic vaginitis
Here's a short post on the pathophysiology of atrophic vaginitis!
