Hypermobility and Neurological Symptoms: Why Different Conditions Can Feel So Similar

A patient guide to hypermobility, MS, small fibre neuropathy, CIDP, CMT, FND and dysautonomia.

People with hypermobile Ehlers-Danlos syndrome (hEDS) and hypermobility spectrum disorder (HSD) can experience a wide range of symptoms involving movement, sensation and nervous system function. Some of these symptoms overlap with those seen in neurological conditions, making it difficult to understand where one explanation ends and another begins.

Weakness, tingling, numbness, balance difficulties and changes in walking can arise through different mechanisms. The way these symptoms feel, when they occur and how they develop over time can provide important information about what may be happening.eryday language, even though different parts of the body may be involved.

Following our previous blog about Christina Applegate's reported MS misdiagnosis, members of our community shared their experiences and mentioned other conditions, including CIDP, Charcot-Marie-Tooth disease, small fibre neuropathy, functional neurological disorder and dysautonomia.

Their comments raised an important question: why can different neurological conditions feel so similar, and how can we understand the differences?

This guide explores four things:

• What symptoms actually feel like: The differences between weakness, instability, fatigue, altered sensation and difficulty controlling movement.

• What may be causing them: How connective tissue, nerves, muscles and the autonomic nervous system contribute to symptoms.

• What investigations can reveal: What MRI, nerve conduction studies, skin biopsies and other assessments measure, including what they may miss.

• How to discuss your symptoms: The details and questions that can make conversations with clinicians more useful.

The goal is to give you practical knowledge, clearer language for describing your experiences and a better understanding of the investigations used to assess them.

Why the connective tissue context matters

hEDS stands for hypermobile Ehlers-Danlos syndrome, and HSD stands for hypermobility spectrum disorder. Both affect several body systems, which helps explain why symptoms extend beyond the joints.

Connective tissue supports structures throughout the body, including ligaments, tendons, muscles and organs. In hEDS/HSD, differences in connective tissue properties can affect joint stability and the way forces move through the body.

Your nervous system also relies on proprioception, the sense that tells you where your body is positioned without looking. It helps you coordinate movement, maintain balance and adjust muscle activity.

When joints are less stable or proprioceptive feedback is altered, muscles need to work harder to control movement. Walking, standing and maintaining posture can become more demanding.

People with hEDS/HSD also experience symptoms involving circulation, digestion, bladder function and sensation. Associated conditions such as dysautonomia and small fibre neuropathy can contribute to these difficulties. The hEDS overview in GeneReviews describes these multisystem features.

This wider context matters because a sensation of weakness can come from several different mechanisms, even within the same person.

“My legs feel weak” can describe different experiences

When you tell a clinician that your legs feel weak, you may be describing very different physical experiences. For example:

• Reduced muscle strength: You struggle to push yourself up from a chair, climb stairs or lift your foot because your muscles cannot produce their usual force.

• Joint instability: Your knees or ankles feel unreliable, as though they might give way while walking or standing.

• Difficulty controlling movement: You struggle to coordinate your steps, place your feet accurately or maintain balance.

• Pain-related difficulty: You can produce the movement, but pain makes you limit it or change how you move.

• Fatigue or heaviness: Your legs become increasingly difficult to move after activity or prolonged standing.

These differences matter. “My legs feel weak after standing for ten minutes” gives different information from “I cannot lift the front of my foot when I walk.” Both descriptions are useful, but they point towards different patterns that a clinician can investigate.

In hEDS/HSD, changes in joint support can increase the muscular effort needed for movement. A study of muscle-tendon mechanics and walking found altered muscle activation and a higher energy cost of walking. Proprioception also influences movement control, as explored in this study of strength, proprioception and activity limitations.

Pain and fatigue can make movement more difficult. Persistent pain can also increase the sensitivity of pain-processing pathways, making ordinary movement or touch feel more painful. This process is called central sensitisation. A study involving people with joint hypermobility syndrome/EDS-hypermobility type identified it as a possible contributor to widespread pain.

Neurological conditions can produce similar experiences through changes in nerve signalling. One of the first distinctions is whether those changes involve the central nervous system or the peripheral nerves.

MS: where are the nerve signals being affected?

Multiple sclerosis (MS) affects the central nervous system: the brain, spinal cord and optic nerves. In MS, immune-mediated inflammation damages myelin, the protective covering around nerve fibres, and can also injure the nerve fibres themselves. This disrupts the signals travelling through affected areas.

The symptoms depend partly on where the damage occurs. MS can cause weakness, altered sensation, visual problems, balance difficulties and bladder symptoms.

Clinicians look closely at which symptoms occurred, how they developed and what the neurological examination shows.

An MRI scan can reveal lesions, which are areas of abnormal tissue signal. Their location and appearance help clinicians assess whether the findings are consistent with MS.

Other conditions, including migraine and small blood vessel disease, can also produce white matter changes. The pattern of lesions therefore matters.

A lumbar puncture may provide additional evidence. Oligoclonal bands are proteins detected in spinal fluid that can indicate immune activity within the central nervous system. They can support an MS diagnosis when considered alongside the history, examination and MRI findings.

NICE guidance on MS diagnosis explains how these findings are combined. Mayo Clinic Laboratories also explains oligoclonal band testing.

The key distinction is where MS causes damage. It affects the brain, spinal cord and optic nerves. Other conditions can cause similar symptoms by affecting the peripheral nerves that connect the central nervous system to the rest of the body.

Small fibre neuropathy: why can routine nerve tests be normal?

Peripheral nerves contain different types of nerve fibres, each with particular functions.

Small nerve fibres carry information about pain and temperature. Some also control automatic functions such as sweating and blood vessel responses. Small fibre neuropathy (SFN) occurs when these fibres are damaged or do not function properly.

People may describe:

• Burning pain: Feet or hands may feel hot, burning or painful even without an obvious external cause.

• Prickling or tingling: Sensations resembling pins and needles, sometimes occurring spontaneously.

• Altered temperature sensation: Difficulty sensing heat or cold, or experiencing temperature changes unusually.

• Reduced sensation: Areas that feel less sensitive than expected.

• Autonomic symptoms: Changes involving sweating, circulation or other automatic functions when autonomic fibres are affected.

The location and pattern of these sensations matter. Symptoms may begin in the feet and move upwards, or follow other distributions.

Several studies have documented SFN in people with hEDS/HSD, including research involving patients referred for suspected small fibre problems and a 2023 skin biopsy study. These studies support an association, although they do not establish how common SFN is across everyone with hEDS/HSD.

Why can nerve conduction studies be normal?

Routine nerve conduction studies mainly measure larger nerve fibres. Small fibres are assessed using different methods. This means someone with isolated SFN may have normal nerve conduction results despite experiencing burning pain, altered temperature sensation or other small fibre symptoms.

A skin biopsy can measure the density of small nerve fibres. A reduced density can support an SFN diagnosis when it matches the symptoms and clinical examination. Other sensory or autonomic tests may provide further information.

The AANEM review of SFN testing discusses these investigations and their limitations.

Identifying SFN may lead to further assessment of possible causes, including metabolic, immune or genetic conditions.

Small fibres mainly carry sensory and autonomic information. Marked loss of muscle strength suggests that other structures or nerve fibres may also be involved.

One condition that can affect the peripheral nerves responsible for muscle activation is CIDP.

CIDP: when inflammation affects peripheral nerves

CIDP stands for chronic inflammatory demyelinating polyradiculoneuropathy.

In CIDP, an abnormal immune response damages myelin around peripheral nerves and nerve roots. This interferes with the electrical signals that allow nerves to communicate with muscles and carry sensory information.

Both MS and CIDP involve demyelination, meaning damage to myelin. The difference is where that damage occurs:

• MS affects the central nervous system.

• CIDP affects the peripheral nervous system.

CIDP can cause progressive or relapsing weakness, altered sensation and difficulty walking. Reflexes are often reduced or absent. Someone may notice increasing difficulty climbing stairs, rising from a chair, lifting their feet or using their hands. Clinicians examine the pattern of weakness, sensory changes and reflexes, as well as how symptoms have developed over time.

Nerve conduction studies help identify characteristic patterns of disrupted signalling, including evidence of demyelination. Testing several nerves can show how widespread the changes are. A lumbar puncture may reveal increased spinal fluid protein, which can provide additional support for the diagnosis.

The European Academy of Neurology and Peripheral Nerve Society CIDP guideline explains how clinicians combine these findings.

Recognising CIDP matters because it is an immune-mediated condition with specific treatment options.

Some inherited neuropathies can produce similar weakness and sensory changes, which brings us to Charcot-Marie-Tooth disease.

CMT: when the peripheral nerve condition is inherited

Charcot-Marie-Tooth disease (CMT) refers to a group of inherited conditions affecting peripheral nerves.

Different genetic changes can affect the nerve fibres themselves, their myelin covering or both. The result is gradually changing nerve function, often beginning in the feet and lower legs.

Common features include:

• Foot drop: Difficulty lifting the front of the foot, which can cause tripping or changes in walking.

• Foot shape changes: High arches or curled toes may develop.

• Muscle wasting: The muscles of the feet and lower legs may become smaller.

• Reduced sensation: Changes in the ability to feel touch or other sensations, particularly in the feet.

• Balance difficulties: Walking on uneven surfaces or in the dark may become more challenging.

Symptoms often progress slowly, sometimes over many years.

Both CMT and CIDP can affect nerve conduction results. The pattern of nerve changes, the pace of progression and the family history help clinicians distinguish them. Genetic testing can identify the cause in some forms of CMT. The results depend on which genes and variants are included in the test.

The NINDS guide to CMT explains its symptoms, diagnosis and management.

CIDP and CMT show why similar weakness can arise from different types of peripheral nerve disease. Identifying the cause helps determine the appropriate treatment and management.

Movement difficulties can also occur through changes in how the brain controls movement, as seen in functional neurological disorder.

FND: what is happening, and what causes it?

Functional neurological disorder (FND) is a recognised neurological condition involving disruption in how brain networks control movement, process sensation or regulate awareness.

It can cause involuntary weakness, tremor, walking difficulties, sensory changes and episodes called functional seizures. Symptoms can significantly affect everyday life.

A person with functional limb weakness may struggle to move a leg when deliberately trying to do so, while showing stronger movement during a different, more automatic action.

Researchers are investigating how attention, sensory information and the brain's predictions about movement interact in FND. A review of FND discusses these developing explanations.

There is no single cause that explains every case. Illness, injury, persistent pain or psychological stress may act as triggers, while some people have no identifiable trigger.

How is FND diagnosed?

Doctors diagnose FND by looking for specific patterns during a neurological examination.

For example, someone may struggle to push their leg down when asked to do so, but the same leg produces more force when they try to lift their other leg against resistance. This is called Hoover's sign.

Why does this matter? It shows that the leg can produce more strength in one situation than another. This difference is a recognised sign of functional leg weakness and helps the neurologist make the diagnosis.

Doctors call findings like this positive clinical signs. They provide evidence of FND during the examination. A normal MRI alone cannot establish the diagnosis.

The 2025 clinical recommendations explain how positive signs contribute to the diagnosis.

In people with hEDS/HSD, pain, altered proprioception and movement-control difficulties may also influence muscle activation. These factors are relevant when assessing how movement is affected.

A small study in selected hEDS/HSD patients explored functional neurological signs and the possibility of coexisting FND.

If FND is proposed, you can ask your clinician which examination findings support the diagnosis and how they relate to your symptoms. Understanding those findings makes the explanation more meaningful.

So far, we have explored conditions involving sensation, muscle activation and movement control. The nervous system also regulates automatic functions, including circulation, which can produce another kind of weakness or physical difficulty.

Dysautonomia: why does standing change how you feel?

The autonomic nervous system regulates functions that happen automatically, including heart rate, blood pressure, sweating and digestion.

Dysautonomia describes problems with this regulation. Autonomic symptoms are common in people with hEDS/HSD.

Someone with autonomic difficulties may experience:

• Lightheadedness or dizziness, especially when standing.

• A racing heart or palpitations when upright.

• Shaky, heavy or weak-feeling legs after standing for a period.

• Blurred vision or difficulty concentrating during upright activity.

• Changes in sweating or temperature tolerance.

These symptoms may be influenced by posture, heat, meals or physical activity.

Where does POTS fit in?

Postural orthostatic tachycardia syndrome (POTS) is one form of orthostatic intolerance involving an excessive sustained rise in heart rate when upright, together with characteristic symptoms.

When you stand, gravity shifts blood towards the lower body. Your autonomic nervous system responds by adjusting heart rate and blood vessel activity to maintain circulation.

In POTS, this response involves an excessive increase in heart rate that meets specific diagnostic criteria.

Other forms of orthostatic intolerance may involve blood pressure changes or different autonomic responses.

A standing or tilt-table test measures heart rate and blood pressure as body position changes. These measurements help clinicians identify the pattern.

The assessment also considers possible contributors such as dehydration, anaemia and medication effects.

The 2026 international consensus discusses patients with significant orthostatic symptoms who fall outside conventional POTS criteria.

For further reading, see the review of dysautonomia in EDS/HSD and the autonomic testing consensus.

The timing of symptoms is particularly useful here. Legs that become heavy and shaky after standing may reflect a different process from legs that struggle to generate force during a strength test.

Recognising these differences helps clinicians choose appropriate investigations.

What each assessment can tell you

A normal test does not always mean there is no problem. Different tests examine different parts of the nervous system. For example, routine nerve conduction studies assess larger nerve fibres, so someone with isolated small fibre neuropathy may have normal results. A skin biopsy or other specialised assessment may provide information about the smaller fibres.

Knowing what a test measures helps you understand what your results tell you and what questions to ask next.

Assessment	What it helps establish	What it may miss or leave unanswered
Neurological examination	Patterns of weakness, reflex changes, altered sensation and movement difficulties.	The exact cause of those findings may require further investigation.
Brain and spinal cord MRI	Structural or inflammatory changes affecting the central nervous system, including lesions relevant to MS.	Problems involving peripheral nerves or autonomic function.
Nerve conduction studies	How larger peripheral nerves transmit signals, including patterns seen in some neuropathies.	Small fibre neuropathy when only small fibres are affected.
Skin biopsy for SFN	Whether small nerve fibre density is reduced in the sampled skin.	The cause of fibre loss, and some cases where symptoms persist despite a normal biopsy.
Genetic testing for neuropathy	Whether an identifiable genetic variant explains an inherited neuropathy.	Genetic causes that are not covered or detected by the test performed.
Standing or tilt-table test	Changes in heart rate and blood pressure when upright, helping assess orthostatic intolerance.	The complete cause of symptoms, which may require additional assessment.

The NINDS explanation of peripheral nerve testing provides further information.

A useful question after any investigation is: “What did this test look for, and does it assess the symptoms I am experiencing?”

When one diagnosis explains only part of your experience

Different symptoms can have different causes, even when they occur in the same person.

For example, someone may have burning feet caused by small fibre neuropathy and also experience dizziness and palpitations when standing because of an autonomic problem.

Both sets of symptoms deserve to be understood.

In hEDS/HSD, joint instability, proprioception, pain and fatigue may interact to affect movement. Peripheral nerve or autonomic conditions may contribute additional difficulties.

Other neurological conditions can also coexist.

Sometimes several symptoms result from interacting mechanisms within one condition. In other cases, more than one diagnosis is needed to explain the findings.

The important question is whether the diagnoses and clinical findings explain the full pattern of symptoms.

That question can help guide further discussions when an explanation feels incomplete.

Making the conversation more useful

The words you use to describe your symptoms can provide important clinical information.

Before an appointment, try to identify three things:

• What does it feel like? Is your leg painful, unstable, heavy, numb, shaky, difficult to control or genuinely unable to produce its usual force?

• When does it happen? Does it occur while walking, climbing stairs, standing still, after exercise or at rest?

• How has it changed? Did it appear suddenly, develop gradually, worsen over weeks or come and go in episodes?

For sensory symptoms, describe whether you experience burning, tingling, reduced sensation or altered temperature sensitivity. Mention where the sensations occur and whether they spread or change.

A short symptom timeline can be useful, particularly if you have seen several specialists. Bring previous reports and include relevant family history, injuries and symptoms involving other body systems.

Questions worth asking your clinician

• Which findings support this diagnosis?

• Which of my symptoms does it explain?

• What did this investigation assess, and what could it miss?

• Are there symptoms or examination findings that need further assessment?

• What are the next steps?

If you are seeking another specialist opinion, copies of previous investigations and a clear explanation of the unresolved question can help the next clinician review your case.

Sudden weakness, new loss of vision or rapidly developing neurological symptoms require urgent medical assessment.

Understanding your symptoms with ParaMotion

Weakness, altered sensation, balance difficulties and fatigue can arise from different processes involving connective tissue, muscles, peripheral nerves, the brain, spinal cord and autonomic nervous system.

The details matter. How a symptom feels, when it appears, how it changes and what investigations reveal can help distinguish between possible explanations.

At ParaMotion, we translate research into practical education for people with hypermobility and associated conditions. We want you to understand the science behind your symptoms, recognise meaningful differences and have the knowledge to take part in informed conversations about your care.

Our individualised movement support considers how joint stability, muscle control, pain, fatigue and associated symptoms influence everyday activities such as walking, standing and maintaining balance.

Explore more patient education and 👉 [Book your Free call here!!] we’ll talk about what’s possible for your body, at your pace.