هذا أعراضه كلش nonspecific
لغرض التبسيط، فهي أما تكون cardiovascular (wet beriberi)
أو تكون neurological (dry beriberi) أو مزيج من الإثنين

• while Guillain-Barré syndrome (GBS) is an important cause of acute flaccid paralysis, thiamine deficiency should be considered an important differential diagnosis, particularly in patients with a history of dietary deprivation and incarceration. 

• high-output cardiac failure should prompt investigation of thiamine deficiency as a cause.

Case 1:

72 year-old male with a history of diabetes and remote Whipple procedure who presented with four weeks of weakness and sensory loss. Exam showed distal sensory loss, mild proximal and distal lower limb weakness, and reduced reflexes. Axonal neuropathy was noted on EMG. CSF showed cytoalbuminologic dissociation. IVIG was initiated for a presumptive diagnosis of GBS. He subsequently developed hypotension requiring pressors, lactic acidosis, encephalopathy, ocular muscle weakness and respiratory failure.

Case 2:

38 year-old male with a history of alcoholism and Crohn's was transferred to the facility with 3-4 weeks of progressive sensory and motor deficits, hypotension, tachycardia, and lactic acidosis attributed to GBS and superimposed sepsis. He subsequently developed severe generalized weakness, respiratory failure, encephalopathy and extraocular muscle paresis. Workup revealed axonal neuropathy, no infection and normal CSF findings.

Diagnosis/Treatment:

In both cases, features of Wernicke's and wet beriberi prompted the clinical suspicion supported by brain MRI studies and reduced thiamine levels (19&23 nmol/liter; normal 80-150nmol/liter). Hypotension and cardiac failure rapidly resolved with thiamine repletion. Ocular muscle weakness and encephalopathy resolved within days, but limb weakness only partially improved.

Normal Brain MRI

In conclusion
A high index of suspicion for thiamine deficiency in patients presenting with progressive neuropathy is important as there is significant overlap with GBS. Development of hypotension, tachycardia, lactic acidosis, mental status changes, or extraocular muscle paresis in cases of possible GBS should prompt consideration of thiamine deficiency.

بعد أكو شغلة

تحملوني

Researches showed that thiamine deficiency is associated with neurological problems, including cognitive deficits. Multiple similarities exist between classical thiamine deficiency and Alzheimer's disease (AD) in that both are associated with cognitive deficits and reductions in brain glucose metabolism. Thiamine-dependent enzymes are critical components of glucose metabolism that are reduced in the brains of AD patients and by thiamine decline, and a decrease in their levels could account for the reduction in glucose metabolism. In preclinical models, reduced thiamine can drive AD-like abnormalities, including memory deficits, neuritic plaques, and hyperphosphorylation of tau. Furthermore, excess thiamine diminishes AD-like pathologies. In addition to dietary deficits, drugs or other manipulations that interfere with thiamine absorption can cause thiamine deficiency. Elucidating the reasons why the brains of AD patients are functionally thiamine deficient and determining the effects of thiamine restoration may provide critical information to help treat patients with AD.

شوفوا هذه الكيس

لاحظ هاوس گللهم انطوها thiamine وبعدين من يتعدل انطوها كيك او ايس كريم، لأن الدماغ يحتاج الـ thiamine بالـ metabolism فإذا ما عوضته أول شي، رح يزيد الـ damage.

في سياق متصل بما انو البارحة امتحنت توليد، وحدة من الـ changes اللي تصير خلال الحمل هي Hyperemesis Gravidarum, فالمريضة رح يصير عدها thiamine deficiency، همين بالـ management ما أنطي glucose اذا ما أعوض الـ thiamine.

Mirror neurons by Cajal

Mirror neurons were discovered at the Università degli Studi di Parma in the 1990s, and first described as nerve cells in the frontal and premotor cortex of macaques that fire both when the monkey performs a movement and when it observes the same movement by another monkey or a human. The presence of a ‘mirror’ system (describing a close match between execution and observation of movements) was then also confirmed in humans, but not in other species, indicating that this might be a peculiar feature of primates. Scientists have theorised that mirror neurons allow understanding of the meaning of another’s actions, and constitute the neural basis of imitation learning and empathy.

“Our work shows that the activation of those neurons in the premotor and motor area is a passive response to the observation of an action,” says Albertini.
"For the first time, a non-matching between observing and executing domains is reported," says Vassilis Raos, associate professor at the University of Crete and co-author of some of the seminal studies on mirror neurons, who was not involved in the study. “This finding opens a new era in studying the fundamental properties of mirror neurons”.
According to Gregory Hickok, a professor of cognitive science at the University of California Irvine and a critic of the original mirror neuron theory, “this is a confirmation that the mirror neuron system is not the basis of action understanding”. The new study, he notes, shows not only that mirror neurons respond to non-biological stimuli, but that these do not even have to include the core actions (here, a kind of grasp) to activate the network.