Anatomy and Physiology

10/02/2026

10/02/2026

Basal Ganglia: Control of Movement and Motor Learning

The basal ganglia are a group of deep brain nuclei involved in the regulation of voluntary movement, posture, and motor coordination. Major components include the caudate nucleus, putamen, and globus pallidus, along with functional connections to the substantia nigra and subthalamic nucleus.

Rather than initiating movement directly, the basal ganglia help refine motor activity, control movement intensity, and support habit learning. They work closely with the cerebral cortex and cerebellum to produce smooth, purposeful actions. Dysfunction in these circuits is linked to movement disorders such as Parkinson’s disease and Huntington’s disease.

07/02/2026

Sciatica can be more than disc impingement or piriformis syndrome
THE ISCHIOFEMORAL IMPINGEMENT ✍️

Ischiofemoral Impingement (IFI) is a rare cause of hip and buttock pain resulting from narrowing of the space between the ischial tuberosity (pelvis) and the lesser trochanter (femur). This constriction compresses the quadratus femoris muscle and occasionally the sciatic nerve. It is commonly seen in middle-aged women, often caused by developmental issues, hip arthritis, or post-operative changes.

01/02/2026

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31/01/2026

What can be seen

Scotty dog sign (neck discontinuity)

This indicates spondylolysis
The adage here is, don't let your dog lose its head

28/01/2026

Understanding Stroke Syndromes and Their Arterial Territories

This detailed illustration maps the brain's blood supply, showing how different arteries nourish specific regions and how blockages can cause distinct stroke syndromes.

(ICA):
A blockage here can cause fluctuating weakness sensory loss, and altered consciousness.

(ACA):
Supplies the medial frontal and parietal lobes infarction may lead to leg predominant weakness and behavioural changes.

(MCA):
divided into M1 and M2 segments:
M1 occlusion: Severe hemiplegia, eye deviation and global aphasia (if left-sided).
M2 divisions: Superior affects speech (Broca's aphasia); inferior causes visual field cuts and sensory deficits.

:
Supply deep brain structures like the basal ganglia damage leads to abulia (lack of willpower) or hemiparesis.


(PCA):
Needs the occipital lobe strokes cause visual field loss, ataxia, or memory issues.

:
Basilar artery & perforators: Can cause "Locked in syndrome" (a rare neurological condition where a person is fully conscious and aware but completely paralyzed, unable to speak or move, except for vertical eye movements and blinking, typically caused by brainstem damage), ataxia or coma.


(PICA):
Linked to Wallenberg syndrome dizziness, hoarseness, and ataxia.

25/01/2026

Brain Circuitry and Mood Regulation
The regulation of mood and reward processing is driven by a sophisticated network of glutamatergic and GABAergic projection neurons that link several key brain regions. Excitatory glutamatergic pathways originate in the frontal cortex, hippocampus, and amygdala, extending to vital hubs such as the nucleus accumbens (NAc), ventral tegmental area (VTA), and hypothalamus. Complementing these are inhibitory GABAergic projections that facilitate communication from the hypothalamus to the cortex, and from the NAc back to the thalamus and VTA. Together, these connections form a dense, interconnected web that governs emotional and behavioral responses.

Structural changes within these specific circuits are closely linked to the pathology of depression. Clinical observations show that depression is associated with reduced brain volume and a marked decrease in glial cell density across several critical areas, including the prefrontal cortex (PFC), anterior cingulate cortex (ACC), hippocampus, and amygdala. These neuroanatomical shifts likely impair the efficiency of the aforementioned projection networks, disrupting the brain's ability to maintain emotional homeostasis and process rewards effectively.

Reference: Sarawagi, A., et al. (2021).

23/01/2026

🧠 WHY NECK INJURIES DISRUPT VISION, BALANCE & BRAIN FUNCTION
(And why symptoms often persist even when imaging looks “normal”)

One of the most misunderstood contributors to dizziness, brain fog, headaches, visual strain, imbalance, and post-concussion symptoms is cervical somatosensory dysfunction.

This graphic explains why.

At The Functional Neurology Center (theFNC), we don’t look at symptoms in isolation. We look at how sensory systems integrate—and what happens when one of the most powerful sensory inputs in the body goes offline.

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🧩 THE STARTING POINT: TRAUMA, STRESS & INFLAMMATION

Many patients we see have a history of:
• Whiplash
• Concussion
• Repetitive micro-trauma
• Chronic stress
• Ongoing pain and inflammation

These stressors don’t just affect tissues—they alter how the nervous system processes information.

One of the first systems to change?
👉 Cervical mechanoreceptors.

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🦴 THE NECK: A MAJOR SENSORY ORGAN (NOT JUST A STRUCTURE)

The upper cervical spine contains an extremely high density of:
• Muscle spindles
• Joint mechanoreceptors
• Proprioceptive afferents

These receptors constantly inform the brain about head position, motion, and spatial orientation.

After injury or chronic stress, these receptors can become:
• Hyper-sensitive
• Inaccurate
• Noisy

This is shown in the graphic as Altered Cervical Mechanoreceptors.

When this happens, the brain is no longer receiving a clean signal from the neck.

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🧠 WHAT HAPPENS NEXT: DISTORTED CERVICAL SOMATOSENSORY INPUT

The brain relies on accurate neck input to correctly integrate:
• Vision
• Balance (vestibular system)
• Posture
• Eye movements

When cervical input is distorted, the brain is forced to re-weight sensory systems, often over-relying on vision or suppressing vestibular input altogether.

This is why patients develop:
• Visual motion sensitivity
• Difficulty focusing or tracking
• Dizziness or imbalance
• Head pressure
• Cognitive fatigue

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👁️🌀 VISUAL & VESTIBULAR SYSTEM DISRUPTION

The graphic shows direct connections from cervical input to:

🔹 Visual System
• Altered reflexes
• Gaze instability
• Eye strain
• Difficulty reading or scrolling

🔹 Vestibular System
• Altered VOR (vestibulo-ocular reflex)
• Balance dysfunction
• Motion intolerance
• Disorientation

These systems are not “broken.”
They are responding to faulty sensory data.

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⚙️ SENSORIMOTOR CONTROL BREAKDOWN

When inaccurate sensory input reaches higher brain centers, the result is:
• Poor sensory integration
• Impaired motor tuning
• Loss of movement precision
• Increased cognitive load

Patients often say:

“I feel disconnected.”
“My body doesn’t trust itself.”
“I’m always bracing.”

That’s not psychological.
That’s sensorimotor mismatch.

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🧠 CNS REORGANIZATION: WHY SYMPTOMS PERSIST

Over time, the brain adapts to distorted input through:
• Altered cortical maps
• Maladaptive movement strategies
• Persistent protective patterns

This explains why:
• MRIs look normal
• Strength tests are fine
• Yet symptoms continue

The issue isn’t damage—it’s dysregulated sensory processing.

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🔁 THE FEEDBACK LOOP (THE PART MOST PLACES MISS)

The graphic highlights a critical loop:
• Poor sensorimotor control → increased stress
• Stress → sympathetic nervous system activation
• SNS activation → increased muscle tone & spindle gain
• Increased spindle gain → worse cervical input

Without targeted neurological care, this loop feeds itself.

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🧠 HOW WE ADDRESS THIS AT theFNC

We don’t chase symptoms.
We correct the sensory signal.

Our approach integrates:
• Cervical proprioceptive retraining
• Visual-vestibular rehabilitation
• Brainstem reflex recalibration
• Neuromodulation (LLLT, ARPwave, tVNS)
• Multisensory integration strategies

This is why many of our patients improve after years of stalled care elsewhere.

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📌 If you’ve been told:
• “Your imaging is normal”
• “It’s just anxiety”
• “You need to rest more”

But your symptoms persist—this model explains why.

🧠 The problem isn’t weakness.
🧠 The problem isn’t motivation.
🧠 The problem is signal quality.

And signal quality can be retrained.

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👉 Learn more at theFNC.com
👉 Share this post if neck injuries, dizziness, or post-concussion symptoms have impacted you or someone you care about

19/01/2026

Neurotransmitters and their hypothetically malfunctioning brain circuits in regions associated with the diagnostic symptoms for depression.
As an personal addition here, it 'just so happens' that these three groups of neurons remove the neurotransmitter from the synapse via presynaptic uptake.

This figure illustrates the major monoamine neurotransmitters involved in depression and the brain circuits through which they contribute to specific symptom domains. The upper panel maps serotonergic, noradrenergic, and dopaminergic projections across key brain regions, including the prefrontal cortex, nucleus accumbens, striatum, amygdala, hypothalamus, thalamus, cerebellum, and spinal cord. Dysfunction within these circuits is linked to characteristic depressive symptoms. Serotonin pathways are primarily associated with mood regulation, guilt, suicidality, appetite, and sleep. Norepinephrine pathways are linked to alertness, energy, psychomotor function, attention, and fatigue. Dopamine pathways play a central role in motivation, pleasure, interest, reward processing, executive function, and psychomotor activity. The figure emphasizes that depression arises from network level disturbances rather than isolated regional defects.

Reference: Lum CT, Stahl SM. Opportunities for reversible inhibitors of monoamine oxidase-A (RIMAs) in the treatment of depression. CNS Specttrums. 2012;17(3):107–120

18/01/2026

How to measure X-rays

When assessing hip pain, instability, femoroacetabular impingement or dysplasia, plain X-rays still matter.
But only if the right lines and angles are understood and interpreted in context.

Here’s what each one is actually looking for ⬇️

🔴 Shenton’s line
Assesses femoral head alignment and overall hip congruency. Disruption can suggest subluxation, dysplasia or fracture patterns.

🔵 Tönnis angle (acetabular roof angle)
Evaluates acetabular inclination and superior coverage. It can be useful when assessing pincer morphology in femoroacetabular impingement, as well as identifying reduced coverage and instability.

🟡 Acetabular index
Measures the slope of the acetabular roof. Larger angles, typically above ~38°, suggest a shallow socket and are commonly associated with dysplasia.

🟢 Femoral neck–shaft angle
Used to assess proximal femoral morphology. This has important implications for hip biomechanics and is also a key parameter in surgical planning for total hip replacement.

🟣 LCEA (lateral centre edge angle)
Assesses lateral acetabular coverage. Low values suggest dysplasia 39°, may be seen in pincer-type femoroacetabular impingement and overcoverage patterns.

🟣 Iliopectineal line
Represents the anterior column of the pelvis and helps assess acetabular and pelvic ring integrity.

🟠 Ilioischial line
Represents the posterior column. Medialisation beyond this line may indicate protrusio acetabuli or structural abnormality.

🔵 Sacral arcuate lines
Used to assess sacral symmetry and neural foraminal alignment. Disruption may indicate sacral pathology or fracture.

📌 None of these measurements should ever be interpreted in isolation.
Symptoms, clinical examination, loading tolerance and patient context always come first.

Lovely job collaborating again with !