2.NEUROLOGY M.SRI SAI PAVAN ROLL NO :79 8TH SEM

A) Link to patient details:                                          

https://143vibhahegde.blogspot.com/2021/05/wernickes-encephalopathy.html

1) what is the evolution of the symptomology in this patient in terms of an event timeline and where is the anatomical localization for the problem and what is the primary etiology of the patient's problem?

Ans: The patient is a chronic alcoholic, he drinks about 3-4quarters/day.he had developed seizures following the cessation of alcohol for 24hours it is due to the following reason:-alcohol affects the way in which nerve cells communicate. receptors are specialized proteins on the surface of nerve cells that receive chemical signals from one another. With long-term alcohol consumption, receptors affected by alcohol undergo adaptive changes in an attempt to maintain normal function.

Two important brain communication systems affected by alcohol involve the neurotransmitters:gamma-aminobutyric acid and glutamate. 

The GABA system:

GABA is an inhibitory neurotransmitter that helps to regulate brain function by rendering nerve cells less sensitive to further signaling. single doses of alcohol facilitate the inhibitory function of the GABA receptor, contributing to alcohol intoxicating effects. During withdrawal, brain GABA levels fall below normal and GABA activity declines. The combination of reduced brain GABA levels and GABAa receptor sensitivity may be contributed an adaptation to the presence of alcohol. In the absence of alcohol, the resulting decrease in inhibitory function may contribute to Symptoms of nervous system hyperactivity associated with both acute and protracted AW.

The glutamate system:

The major excitatory neurotransmitter in the brain is glutamate, which communicates with three major subtypes of glutamate receptors. Among these, the N-methyl-D-aspartate (NMDA) receptor plays a role in memory, learning, and the generation of seizures. Alcohol inhibits the excitatory function of the NMDA receptor in laboratory studies at concentrations associated with mild to moderate alcohol intoxication in humans. As with the increased inhibitory function of the GABAA receptor, the decreased excitatory function of the NMDA receptor is consistent with alcohol’s general sedative effect. Long-term alcohol administration produces an adaptive increase in the function of NMDA receptors. Acute AW activates glutamate systems. In turn, AW seizures are associated with increased NMDA receptor function. Persistent alterations in NMDA receptor function may potentiate the neurotoxic and seizure-inducing effects of increased glutamate release during withdrawal.

The symptom: irrelevant talking, decreased food intake, tremors, sleep disturbance is due to the following reason: chronic alcohol consumption causes thiamine deficiency due to impaired absorption of thiamine from the intestine, a possible genetic predisposition, inadequate diet, reduced storage of thiamine in the liver and other nutritional deficiencies.

THE PATHOPHYSIOLOGY:

Thiamine, one of the first B vitamins to be discovered also known as Vitamin B1, is a coenzyme that is essential for intricate organic pathways and plays a central role in cerebral metabolism. This vitamin acts as a cofactor for several enzymes in the Krebs cycle and the pentose phosphate pathway, including alpha-keto-glutamic acid oxidation and pyruvate decarboxylation. Thiamine-dependent enzymes function as a connection between glycolytic and citric acid cycles. Therefore, deficiency of thiamine will lead to decreased levels of alpha-keto-glutarate, acetate, citrate, acetylcholine and accumulation of lactate and pyruvate. This deficiency can cause metabolic imbalances leading to neurologic complications including neuronal cell death. Neuronal death in the mammillary bodies and thalamus were implicated in multiple cases of Wernicke encephalopathy studied. Studies involving computed tomography (CT) and magnetic resonance imaging (MRI) of patients with Wernicke encephalopathy revealed lesions in the thalamus with dilated ventricles and volume loss in the mammillary bodies. The lesions are usually symmetrical in the midbrain, hypothalamus, and cerebellum.   

The kidneys have an important job as a filter for harmful substances .alcohol causes changes in the function of the kidneys and makes them less able to filter the blood .alcohol also affects the ability to regulate fluid and electrolytes in the body. In addition, alcohol can disrupt hormones that disrupt hormones that affect kidney function .people who drink too much are more likely to have high blood pressure. High blood pressure is a common cause of kidney disease. The increase in levels of urea, creatinine, uric acid leads to uraemic encephalopathy. which causes asterixis.

the deficiency of thiamine and increase in levels of toxins in the body due to renal disease is the primary etiology of the patient's problem.

2)what are the mechanism of action, indication, and efficacy over placebo of each of the pharmacological and nonpharmacological interventions used for this patient?

Ans: I) Thiamine helps the body cells change carbohydrates into energy. It has been used 

as a supplement to cope with thiamine deficiency

ii)Lorazepam binds to benzodiazepine receptors on the postsynaptic GABA-A ligand-gated chloride channel neuron at several sites within the central nervous system.it enhances the inhibitory effects of GABA, which increases the conductance of chloride ions into the cell

iii)pregabalin subtly reduces the synaptic release of several neurotransmitters, apparently by binding to alpha2-delta subunits, and possibly accounting for its actions invivo to reduce neuronal excitability and seizures.

iv)Lactulose is used in preventing and treating clinical portal-systemic encephalopathy .its chief mechanism of action is by decreasing the intestinal production and absorption of ammonia.

v)Potchlor liquid is used to treat low levels of potassium in the body.

3)why have neurological symptoms appeared this time, that were absent during withdrawal earlier ? what could be a possible cause for this time?

Due to excess thiamine deficiency and excess toxins accumulation due to renal disease caused by excess alcohol addiction.

4)what is the reason for giving thiamine in this patient?

 chronic alcohol consumption causes thiamine deficiency due to impaired absorption of thiamine from the intestine,Thiamine, one of the first B vitamins to be discovered also known as Vitamin B1, is a coenzyme that is essential for intricate organic pathways and plays a central role in cerebral metabolism. This vitamin acts as a cofactor for several enzymes in the Krebs cycle and the pentose phosphate pathway, including alpha-keto-glutamic acid oxidation and pyruvate decarboxylation. Thiamine-dependent enzymes function as a connection between glycolytic and citric acid cycles. Therefore, deficiency of thiamine will lead to decreased levels of alpha-keto-glutarate, acetate, citrate, acetylcholine, and accumulation of lactate and pyruvate. This deficiency can cause metabolic imbalances leading to neurologic complications including neuronal cell death. 

5)what is the probable cause for kidney injury in this patient?

 The kidneys have an important job as a filter for harmful substances .alcohol causes changes in the function of the kidneys and makes them less able to filter the blood .alcohol also affects the ability to regulate fluid and electrolytes in the body. In addition, alcohol can disrupt hormones that disrupt hormones that affect kidney function .people who drink too much are more likely to have high blood pressure. High blood pressure is a common cause of kidney disease.

6)what is the probable cause for the normocytic anaemia?

alcohol causes iron deficiency or iron overload due its affect on production of new blood cells organs i.e,bonemarrow and the metabolism of iron .alocohol causes a affect on progenitor cells of blood causing decreased WBC .RBC.alochol decreases iron absorption from intestine .

7)could chronic alcohlism have aggravated the foot ulcer formation ?if yes and why ?

yes,As the patient is diabetic the chance of ulcer formation increases .in a patient of chronic alcoholic theimmune system is weak due to the affect on blood cells formation and iron absorption.due to this healing of an ulcer dampens.

B) Link to patient details:

https://kausalyavarma.blogspot.com/2021/05/a-52-year-old-male-with-cerebellar.html?m=1

1)      What is the evolution of the symptomology in this patient in terms of an event timeline and where is the anatomical localization for the problem and what is the primary etiology of the patients problem?

ANS. Timeline of the patient is as follows-

7 days back- Patient gave a history of giddiness that started around 7 in the morning; subsided upon taking rest; associated with one episode of vomiting

4 days back- Patient consumed alcohol; He developed giddiness that was sudden onset, continuous and gradually progressive. It increased on standing and while walking.

H/O postural instability- falls while walking

Associated with bilateral hearing loss, aural fullness, presence of tinnitus

Associated vomiting- 2-3 episodes per day, non projectile, non bilious without food particles

Present day of admission- Slurring of speech, deviation of mouth that got resolved the same day

Anatomical location- There is a presence of an infarct in the inferior cerebellar hemisphere of the brain.

Etiology- Ataxia is the lack of muscle control or co-ordination of voluntary movements, such as walking or picking up objects. This is usually a result of damage to the cerebellum (part of the brain that controls muscle co-ordination)

Many conditions cause cerebellar ataxia- Head trauma, Alcohol abuse, certain medications eg. Barbituates, stroke, tumours, cerebral palsy, brain degeneration etc.

In this case, the patient has hypertension for which he has been prescribed medication that he has not taken. Stroke due to an infarct can be caused by blockade or bleeding in the brain due to which blood supply to the brain is decreased, depriving it of essential oxygen and nutrients. This process could’ve caused the infarct formation in the cerebellar region of the brain, thus causing cerebellar ataxia.

2)      What are the mechanism of action, indication and efficacy over placebo of each of the pharmacological and non pharmacological interventions used for this patient?

ANS. 

A)     Tab Vertin 8mg- This is betahistine, which is an anti- vertigo medication

MOA- It is a weak agonist on H1 receptors located on blood vessels of the inner ear. This leads to local vasodilation and increased vessel permeability. This can reverse the underlying problem. 

Indications- Prescribed for balance disorders. In this case it is used due to patients history of giddiness and balance issues.

 

B)     Tab Zofer 4mg- This is ondanseteron- It is an anti emetic

MOA- It is a 5H3 receptor antagonist on vagal afferents in the gut and they block receptors even in the CTZ and solitary tract nucleus.

Indications- Used to control the episodes of vomiting and nausea in this patient.

 

C)      Tab Ecosprin 75mg- This is aspirin. It is an NSAID

MOA- They inhibit COX-1 and COX-2 thus decreasing the prostaglandin level and thromboxane synthesis

Indications- They are anti platelet medications and in this case used to prevent formation of blood clots in blood vessels and prevent stroke.

D)     Tab Atorvostatin 40mg- This is a statin

MOA- It is an HMG CoA reductase inhibitor and thus inhibits the rate limiting step in cholesterol biosynthesis. It decreases blood LDL and VLDL, decreases cholesterol synthesis, thus increasing LDL receptors in liver and increasing LDL uptake and degeneration. Hence plasma LDL level decreases.

Indications- Used to treat primary hyperlipidemias. In this case it is used for primary prevention of stroke.

E)      Clopidogrel 75mg- It is an antiplatelet medication

MOA- It inhibits ADP mediated platelet aggregation by blocking P2Y12 receptor on the platelets.

Indications- In this case it decreases the risk of heart disease and stroke by preventing clotting

F)      Thiamine- It is vitamin B1

It is naturally found in many foods in the human diet. In this case, the patient consumes excess alcohol- so he may get thiamine deficiency due to poor nutrition and lack of essential vitamins due to impaired ability of the body to absorb these vitamins.

Indications- Given to this patient mainly to prevent Wernickes encephalopathy- that can lead to confusion, ataxia and opthalmoplegia.

G)     Tab MVT- This is methylcobalamin

Mainly given in this case for vitamin B12 deficiency.

 

3)      Did the patients history of denovo hypertension contribute to his current condition?

 

ANS. A cerebellar infarct is usually caused by a blood clot obstructing blood flow to the cerebellum. High blood pressure that is seen in hypertension (especially if left untreated) can be a major risk factor for the formation of cerebellar infarcts. 

Increased shear stress is caused on the blood vessels. The usual adaptive responses are impaired in this case, thus leading to endothelial dysfunction in this case. High BP can also promote cerebral small vessel disease. All these factors contribute to eventually lead to stroke. 

 

4)      Does the patients history of alcoholism make him more susceptible to ischaemic or haemorrhagic stroke?

 

ANS. Meta analysis of the relation between alcohol consumption and increased risk of stroke has mainly weighed in to the formation of two types- ischaemic and haemorrhagic stroke.

Ischaemic stroke- this is more common. This Is caused by a blood clot blocking the flow of blood and preventing oxygen from reaching the brain

Haemorrhagic stroke- occurs when an aneurysm bursts or when a weakened blood vessel leaks, thus causing cerebral haemorrhage

According to a Cambridge study, heavy drinkers have 1.6 more chance of intracerebral haemorrhage and a 1.8 increased chance of subaracnoid haemorrhage. The adverse effect on BP that is seen due to increased drinking is a major stroke risk factor and increase the risk of heart stroke.

Many studies show that with mild and moderate drinking . the risk of ischaemic stroke decreases due to decreased level of fibrinogen which helps in the formation of blood clots. However, heavy alcohol intake is associated with impaired fibrinolysis, increased platelet activation and increased BP and heart rate. 

So In this case, his history of alcoholism, coupled with his hypertension definitely could be a causative factor of his current condition.

C) Link to patient details:

http://bejugamomnivasguptha.blogspot.com/2021/05/a-45-years-old-female-patient-with.html

1.What is the evolution of the symptomatology in this patient in terms of an event timeline and where is the anatomical localization for the problem and what is the primary etiology of the patient's problem?

A) *Evolution of symptoms :patient was normal 8 months back then developed b/l pedal edema which gradually progressed.

Aggerevated in sitting and standing position, relived on taking medication

*Palpitations :since 5days, sudden in onset which is more during night

Aggerevated by lifting heavy weights, speaking continuously

*Dyspnoea during palpitations (NYHA-3) since 5 days

*pain:since 6days, radiating along left upper limb, more during palpitations and relived on medication.

Chest pain associated with chest heaviness since 5 days

Anatomical localisation :

Palpitations

Dyspnoea(NYHA-3)

Pedal edema

Chest pain

Radiating pain along her left upper limb

Etiological agent :

*By localization, electrolyte imbalance (hypokalemia) causing the her   manifestations like palpitations, chest heaviness, generalised body weak   ness

*radiating pain along her left upper limb due to cervical spondylosis 

2Q) What are the reasons for recurrence of hypokalemia in her? Important risk factors for her hypokalemia? 

A) Reason: recurrent hypokalemic periodic paralysis 

Current risk factor:due to use of diuretics

Other risk factors 

A) Abnormal loses:

Medications-diuretics, laxatives, enema, corticosteriods

Real causes- osmotic diuresis, mineralo corticoid excess, renal tubular acidosis, hypomagnesenemia 

B) trance cellular shift : alkalosis, thyrotoxicosis, delirium tremans, head injury, Myocardial, ischemia, recurrent hypokalemic periodic paralysis

C) Inadequate intake: anorexia, dementia, stareation, total parental nutrition

D) psuedohypokalemia:delayed sample analysis, significant leukocytosis

3) What are the changes seen in ECG in case of hypokalemia and associated symptoms?

A) changes seen in ECG : 

Earliest change :decreased T-wave amplitude, ST depression, Twave - and inversion or flat;prolonged PR interval;presence of Uwaves 

In Severe cases :ventricular fibrillation, rarely AV block 

Symptoms of hypokalemia :

Weakness & fatigue, palpitations, muscle cramps & pain, anxiety, psychosis, depression, delirium.

D) Link to patient details:

https://rishikoundinya.blogspot.com/2021/05/55years-old-patient-with-seizures.html

QUESTIONS:

1.Is there any relationship between occurrence of seizure to brain stroke. If yes what is the mechanism behind it?

seizures after ischaemic strokes. An increase in intracellular Ca2+ and Na+ with a resultant lower threshold for depolarisation, glutamate excitotoxicity, hypoxia, metabolic dysfunction, global hypoperfusion, and hyperperfusion injury 

Seizures after haemorrhagic strokes are thought to be attributable to irritation due to (hemosideri. Deposits)caused by products of blood metabolism

Late onset seizures are associated with the persistent changes in neuronal excitability and gliotic scarring is most probably the underlying cause. 

2. In the previous episodes of seizures, patient didn't loose his consciousness but in the recent episode he lost his consciousness what might be the reason?

Initially the patient might have had Simple partial seizures (no loss of consciousness) and might have progressed to Generalised Tonic Clonic seizures (loss of consciousness)

E) Link to patient details:

https://nikhilasampathkumar.blogspot.com/2021/05/a-48-year-old-male-with-seizures-and.html?m=1

Questions: 1) What could have been the reason for this patient to develop ataxia in the past 1 year?

The patient has minor unattended head injuries in the past 1 yr. Accoding to the CT scan, the patient has cerebral haemorrhage in the frontal lobe causing probably for the occurrence of Frontal lobe present should have been cured on their own. But the patient is a chronic alcholic. This might have hindered the process of healing or might have stopped the healing rendering it to grow further more into 13 mm sized hemorrhages occupying Frontal Parietal and Temporal lobes

2) What was the reason for his IC bleed? Does Alcoholism contribute to bleeding diatheses ?

The patient has minor unattended head injuries. During the course of time the minor hemorrhages if present should have been cured on their own. But the patient is a chronic alcholic. This might have hindered the process of healing or might have stopped the healing rendering it to grow further more into 13 mm sized hemorrhages occupying Frontal Parietal and Temporal lobes

F) Link to patient details:

http://shivanireddymedicalcasediscussion.blogspot.com/2021/05/a-30-yr-old-male-patient-with-weakness.html

Questions

1.Does the patient's  history of road traffic accident have any role in his present condition?

The closeness of facial bones to the cranium would suggest that there are chances of cranial injuries. Since the Zygomatic arch and Mandibular process is very close to the cranium, this might play a role in the patient's present condition

2.What are warning signs of CVA?

Weakness or numbness of the face, arm or leg, usually on one side of the body

Trouble speaking or understanding

Problems with vision, such as dimness or loss of vision in one or both eyes

Dizziness or problems with balance or coordination

Problems with movement or walking

Fainting or seizure

Severe headaches with no known cause, especially if they happen suddenly

3.What is the drug rationale in CVA?

Mannitol- Because of its osmotic effect, mannitol is assumed to decrease cerebral edema. Mannitol might improve cerebral perfusion by decreasing viscosity, and as a free-radical scavenger, it might act as a neuroprotectant. 

Ecospirin 

For the prevention of heart attack, stroke, heart conditions such as stable or unstable angina (chest pain) due to a blood clot.

Atrovas-Atorva 40 Tablet belongs to a group of medicines called statins. It is used to lower cholesterol and to reduce the risk of heart diseases. Cholesterol is a fatty substance that builds up in your blood vessels and causes narrowing, which may lead to a heart attack or stroke.

Rt feed RT feed is a nursing procedure to provide nutrition to those people who are either unable to obtain nutrition by mouth or are not in a state to swallow the food safely. 

4. Does alcohol has any role in his attack?

When the patient met with an accident there might be cranial damage which was unnoticed.

If so his occasional drinking may or may not have hindered the process of the minor hemorrhages getting healed and might have caused this condition

But since the patient is not a chronic alcoholic and so Alcohol might not have played any role.

Therefore it cannot be evaluated without further details

5.Does his lipid profile has any role for his attack??

The inverse relationship between serum HDL-C and stroke risk . When taken together it seems clear that higher baseline levels of serum HDL-C lower the risk of subsequent ischemic stroke.

G) Link to patient details:

https://amishajaiswal03eloggm.blogspot.com/2021/05/a-50-year-old-patient-with-cervical.html                  1.what is myelopathy hand?                                                                              There is loss of power of adduction and extension of the ulnar two or three fingers and an inability to grip and release rapidly with these fingers. These changes have been termed "myelopathy hand" and appear to be due to pyramidal tract involvement. 

2.what is finger escape?

Finger escape

Wartenberg's sign is a neurological sign consisting of involuntary abduction of the fifth (little) finger, caused by unopposed action of the extensor digiti minimi. . This finding of weak finger adduction in cervical myelopathy is also called the "finger escape sign".

3.what is Hoffman's sign?

Hoffman's sign or reflex is a test used to examine the reflexes of the upper extremities. This test is a quick, equipment-free way to test for the possible existence of spinal cord compression from a lesion on the spinal cord or another underlying nerve condition

H) Link to patient details:

https://neerajareddysingur.blogspot.com/2021/05/general-medicine-case-discussion.html?m=1                  ossible questions: 

1) What can be  the cause of her condition ? 

Ans; Presence of cortical vein thrombosis with hemorrhagic venous infarction in right posterior temporal lobe and also Iron deficiency anaemia

2) What are the risk factors for cortical vein thrombosis?

  Ans; For children and infants Problems with the way their blood forms clots

          Sickle cell anemia

         Chronic hemolytic anemia

         Beta-thalassemia major

         Heart disease — either congenital (you're born with it) or acquired (you develop it)

          Iron deficiency

           Certain infections

            Dehydration

            Head injury 

             For newborns, a mother who had certain infections or a history of infertility 

            For adults

            Pregnancy and the first few weeks after delivery

             Problems with blood clotting; for example, antiphospholipid syndrome, protein C and S deficiency, antithrombin III deficiency, lupus anticoagulant, or factor V Leiden mutation

        Cancer

      Collagen vascular diseases like lupus, Wegener’s granulomatosis, and Behcet syndrome

       Obesity

      Low blood pressure in the brain (intracranial hypotension)

    Inflammatory bowel disease like Crohn’s disease or ulcerative colitis

 

3)There was seizure free period in between but again sudden episode of GTCS why?resolved spontaneously  why?  

   Ans   Missed medication

           Lack of sleep

            Stress

           Menstruation About half of women of childbearing age with epilepsy have increased seizures around their period. This is most likely due to hormonal changes that occur during your monthly cycle.

      Herbal medications — as well as the herbs that go into many dietary supplements — can actually cause seizures or worsen side effects of seizure medication. The same goes with essential oils. Certain ones, such as juniper and umbrella plant, have been known to induce seizures.

       Vitamin B6 (pyridoxine) deficiency is the only type of vitamin deficiency that’s been proven to potentially cause or worsen seizures

4) What drug was used in suspicion of cortical venous sinus thrombosis?

 

Ans ; Inj sodium valproate and Inj phenytoin have anti platlet activity