Dr. Muhammad Asif Khaskheli

22/08/2025

Did you know your forebrain is the command center of sleep? 🧠

While you drift off, your brain is running one of the most complex programs in nature:

✨ Prefrontal Cortex – regulates decision-making & emotional control during sleep.
✨ Thalamus – gates sensory input, controlling NREM rhythms.
✨ Hippocampus – consolidates memories overnight.
✨ Hypothalamus – sets your circadian clock and flips the sleep–wake switch.
✨ Basal Forebrain – helps you transition into deep sleep.

Most people think sleep is just “rest.” But here’s the truth:
When you close your eyes, an entire battle of brain circuits begins inside your head. ⚡

✨ The Basal Forebrain flips between two modes; cholinergic neurons keep you alert, while GABA neurons pull you into deep sleep.
✨ The Hypothalamus acts like a switch:

- VLPO = your sleep button 😴
- Orexin neurons = your wake button ☀️

✨ The Thalamus? It shuts the gates of sensory overload, letting you disconnect from the outside world.
✨ And the Cortex, it doesn’t sleep. It rewires itself, strengthens memories, and even dreams.

So when you're sleeping, remember your brain is hard at work, running one of the most sophisticated programs nature ever designed.

💡 Question for you: Do you usually feel more refreshed after a deep night’s sleep or after a short nap? Comment below.

20/08/2025

Dystrophinopathies

18/08/2025

Harvard Medical School scientists have made a groundbreaking discovery linking lithium to Alzheimer’s disease treatment. Their research found that lithium levels are significantly lower even in the earliest stages of memory loss. Amyloid-beta plaques, known to cause Alzheimer’s, bind to lithium in the brain, reducing its availability and speeding up the disease’s progression.

This study marks the first time lithium, widely used in psychiatric medicine, has been shown to naturally exist in the brain at important biological levels. In mouse models, lithium depletion caused a rapid buildup of harmful amyloid-beta and tau proteins, increased brain inflammation, and worsened cognitive decline.

The breakthrough came when researchers used lithium orotate, a form of lithium that avoids binding with amyloid-beta plaques. At very low doses, lithium orotate reversed memory loss and other Alzheimer’s-like symptoms in mice without any toxicity. While human trials are still needed, this discovery opens the door to lithium testing as a way to identify people at risk and the potential for targeted lithium supplementation to prevent or even restore cognitive function in dementia patients.

This exciting development could transform the future of Alzheimer’s treatment and prevention, offering new hope to millions worldwide.

17/08/2025

fans

Approach to a Floppy Infant:::

When evaluating a floppy (hypotonic) infant, it is important to consider congenital myopathies and muscular dystrophies among the differential diagnoses.

Ptosis is an important clinical clue:
Seen in congenital myotonic dystrophy and transient neonatal myasthenia gravis.

Congenital myotonic dystrophy features:
Ptosis
Elongated face
Hollow cheeks
Tented upper lip
Open mouth posture
Associated with maternal history of myotonia

Nemaline (rod) myopathy:
Open mouth due to facial muscle weakness, especially involving jaw closure.

Centronuclear (myotubular) myopathy:
Presents with ptosis, cryptorchidism (undescended te**es), and may have doses of mitochondrial dysfunction if of the mitochondrial subtype.

Central core disease / multiminicore disease:
Associated with susceptibility to malignant hyperthermia.

SEPN1-related myopathy (selenoprotein N1 deficiency):
Presents with rigid spine, axial weakness, and respiratory involvement.

Congenital muscular dystrophies:
Features include hypotonia, contractures, elevated CPK, eye involvement, and importantly, brain abnormalities, such as lissencephaly and other structural brain malformations (especially in dystroglycanopathies).

Spinal Muscular Atrophy (SMA) type 1:
Severe hypotonia, paradoxical (abdominal) breathing, and tongue fasciculations; CPK is normal or mildly elevated.

Other causes of neonatal hypotonia or hypertonia include:
Down syndrome
Prader-Willi syndrome
Birk-Barel syndrome
Sepsis
Hypoxic-ischemic encephalopathy
CNS malformations or metabolic disorders

17/08/2025

Understanding how cranial nerves impact swallowing is essential for recognising the root causes of difficulties with speech, eating, and oral motor function. This diagram highlights the key cranial nerves involved in the swallowing process, Trigeminal (V), Facial (VII), Glossopharyngeal (IX), Vagus (X), and Hypoglossal (XII), and explains what happens when each is damaged.

17/08/2025

17/08/2025

fans
Dr. Kashif khaskheli

17/08/2025

Get your blood pressure checked at least once a year and understand what the numbers mean. Severe high blood pressure combined with symptoms such as chest pain or trouble speaking may be a hypertensive emergency, according to the new high blood pressure guideline.

16/08/2025

Scientists officially name malnutrition-linked diabetes as type 5.

A newly recognized form of diabetes, called type 5, has been classified by the International Diabetes Federation. It is caused by poor nutrition early in life, especially a lack of protein during key growth periods, which limits the development of insulin-producing cells in the pancreas.

Type 5 differs from type 1, where the immune system destroys these cells, and from type 2, which is often linked to weight and lifestyle. Studies in animals have shown how low-protein diets during pregnancy or adolescence can stunt pancreas growth, and similar effects are now confirmed in humans. The condition is most common in low-income regions and may affect up to 25 million people worldwide.

FOLLOW
Dr. Muhammad Asif Khaskheli
For more update

15/08/2025

Parinaud Syndrome (Dorsal Midbrain Syndrome): Clinical Features and Neuroanatomical Basis

Definition:
Parinaud syndrome, also known as dorsal midbrain syndrome or pretectal syndrome, is a cluster of ocular motor and pupillary abnormalities caused by lesions affecting the dorsal midbrain near the pretectal area. It is most commonly associated with compression or ischemia involving the posterior commissure, superior colliculi, and adjacent structures.

Etiology

Lesions leading to Parinaud syndrome typically involve:

1. Mass Effect (most common):

◦ Pineal region tumors (e.g., germinoma, pineoblastoma)

◦ Hydrocephalus (3rd ventricular dilation compressing the midbrain)

◦ Thalamic or midbrain hemorrhages

2. Vascular Causes:

◦ Posterior cerebral artery (PCA) or thalamoperforator infarcts

3. Inflammatory/Demyelinating:

◦ Multiple sclerosis (rare)

◦ Neurosarcoidosis

4. Infectious/Traumatic:

◦ Midbrain encephalitis

◦ Traumatic brain injury

Clinical Features (Classic Triad + Associated Signs)

1. Vertical Gaze Palsy

◦ Upgaze limitation (most prominent) due to disruption of the rostral interstitial nucleus of the medial longitudinal fasciculus (riMLF) and posterior commissure.

◦ Downgaze palsy (less common, suggests more extensive damage).

◦ Bell’s phenomenon (reflexive upward eye movement on eyelid closure) may be preserved.

2. Convergence-Retraction Nystagmus

◦ Attempted upgaze triggers converging and retracting eye movements due to co-contraction of extraocular muscles (mediated by aberrant signals in the pretectal area).

◦ Best elicited with downward-moving optokinetic (OKN) stimuli.

3. Pupillary Light-Near Dissociation

◦ Pupils are mid-dilated and poorly reactive to light but constrict during accommodation (near reflex).

◦ Caused by disruption of the pretectal olivary nucleus (light reflex) with sparing of the Edinger-Westphal nucleus (near reflex).

4. Additional Features (Depending on Lesion Extent)

◦ Eyelid retraction (Collier’s "tucked lid" sign) – Due to disinhibition of the levator palpebrae.

◦ Convergence spasm or palsy

◦ Skew deviation (if the interstitial nucleus of Cajal is involved).

Diagnosis and Imaging

1. Neuroimaging (MRI preferred):

◦ T1/T2-weighted MRI to assess for pineal masses, hydrocephalus, or infarcts.

◦ Contrast-enhanced studies if tumor or inflammatory etiology is suspected.

2. Lumbar puncture (if hydrocephalus or infection is suspected).

3. Serum/CSF markers (e.g., beta-hCG, AFP for germ cell tumors).

Differential Diagnosis

• Progressive supranuclear palsy (PSP) – Mimics vertical gaze palsy but lacks convergence-retraction nystagmus.

• Myasthenia gravis – Fatigable ptosis/ophthalmoplegia without midbrain signs.

• Thalamic syndromes – May affect vertical gaze but usually with sensory/motor deficits.

Management

1. Treat Underlying Cause:

◦ Surgical decompression/resection (e.g., pineal tumor).

◦ Ventriculoperitoneal shunt for obstructive hydrocephalus.

◦ Immunotherapy if demyelinating/inflammatory.

2. Symptomatic Therapy:

◦ Prisms for diplopia.

◦ Botulinum toxin for severe convergence spasm.

Prognosis

• Reversible if due to transient compression (e.g., hydrocephalus).

• Persistent deficits if infarction or infiltrative tumor is present.

14/08/2025

A revolutionary therapy using stem cells to repair damaged nerves has entered human trials, offering hope for millions living with paralysis. The treatment involves injecting specialized cells into the spinal cord to regenerate nerve pathways.

Early results in animal models have shown restored movement and sensation, making this one of the most promising developments in regenerative medicine. If successful, it could transform treatment for spinal cord injuries caused by accidents, strokes, or degenerative diseases.

The trials will determine safety, efficacy, and long-term benefits, potentially leading to a medical breakthrough within the decade.