CASE PRESENTATION
BY
TOKS-OMAGE ESELOBU 190705081
ONIFADE OPEOLUWA BISOLA 210701504
OLOGUN RUTH OLUWAPELUMI 190701017
AJEWOLE TAIWO
Name: Abachukwu
Tobechukwu Godwin
Age: 27
Sex: Male
Address: 19, Bishop
Amsterdam, Abule Ado,
Lagos
Biodata
Religion: Christian
Occupation: Copper
Marital status: Single
Ethnicity: Igbo
PRESENTING COMPLAINT
● Change in voice 4/12
● Blurry vision 4/12
● Progressive limb
weakness 3/12
HISTORY OF PRESENTING COMPLAINT
● Patient was in his usual state of health until 4/12
when he noticed his inability to hit certain notes
when he sang.
● This was associated with a tingling sensation which
was felt all over his body and was noticed to become
worse on strenuous exercise.
● After a month he realized that he could not read texts
on his phone.
● His text on his phone which was normal to him
became very tiny and he had to increase the text size.
● He also realized that he could not read subtitles on
movies he was watching.
● It progressed to being unable to see anything clearly,
his vision became blurry.
● During the same period, he started feeling
weakness in his lower limbs which was
accompanied with a feeling of heaviness in both
lower limbs and this made it necessary for him to
be assisted in order to move.
● It got to the point when he could not put on his
slippers on his feet.
● Patient also developed difficulty swallowing
especially liquids and there was occasional
choking during meals.
● This progressive weakness was not associated
with loss of sphincteric control and bowel control
and he was able to feel touch and pain.
● At this point he had to be taken to the hospital at Delta
where he was serving.
● At the hospital he was admitted with painkillers and
drips, he mentioned that he saw improvements but
noted that he got tired after strenuous work.
● He mentioned that he was asked to engage in
physiotherapy sessions of which he had five.
● He noticed a rapid decline during the course of the
session which lasted for about two weeks.
● Due to constraint and limited resources the hospital referred him to
Delta state teaching hospital but because of a strike ongoing he was
referred to Lagos.
● A night before getting to Lagos he noticed weakness in his hands but
was still able to use his phone.
● This was first week in December . On getting to Lagos, he went to
Igbobi where he was asked to see a neurologist. He went to FMC
where he was unable to see a neurologist till the festive period.
● During that period he experienced shortness of
breath ??? and had to be taken to a private hospital.
● The neurologist at Isolo then referred him to
neurology unit at LUTH for a second opinion.
● 2/7 he was brought into the ward to commence test
and treatments.
● No history of similar
illness in the past.
● No history of chronic
diseases e.g DM,
SCD,HTN,asthma,seizur PAST MEDICAL
e disorder, PUD.
HISTORY
● No history of previous
hospital admission,blood
transfusion or surgery.
● No history of similar illness
in the family.
● No history of chronic
diseases in the family e.g FAMILY
DM,
SCD,HTN,asthma,seizure HISTORY &
disorder, PUD.
DRUG HISTORY
● No significant drug history,
no chronic drug use and drug
allergies.
●
● CNS: Blurry vision
● RS: Shortness of breath
● MUSCULOSKELETAL:
Difficulty in walking, REVIEW OF
muscle weakness.
SYSTEMS
● No other significant findings
in the other systems
●
●
●
●
SUMMARY
A 27 year old male, with no background history of chronic illness.
Worsening blurry vision, shortness of breath and progressive limb weakness of 4 months
duration
He was referred to LUTH for proper investigation and expert care..
He was admitted into the ward where he received care, had a number of investigations
done and received medication.
On commencement of treatment we saw that his facial muscles became less weak and
his hand movement improved particularly on the right.
Patient was discharged on the 18th of january,2025 with plans to commence
plasmapheresis.
General Physical Examination
●
● A young male, not in any obvious distress, afebrile, not pale,
anicteric, acyanosed, not dehydrated, no obvious lymph node
enlargement, no pedal edema.
Cardiovascular System CNS EXAMINATION
On Admission Conscious and alert. Oriented in time, person and
place No evidence of cranial nerve palsy Tone,
Pulse: 106bpm, irregular, full volume, with thickened power, and reflexes were normal in all limbs
arterial wallAbsent locomotor brachialisBP: 126/98
mmHgJVP: not elevatedApex beat: 5th left IC, Presently:Pulse: 75bpm, regular, full volumeBP:
lateral to the mid-clavicular lineHeart sounds: S1, S2; 127/82 mmHg
no added sounds
ABDOMINAL ABDOMINAL
EXAMINATION EXAMINATION
Abdomen was uniformly distended moves with Abdomen was uniformly distended moves with
respiration, no scars, umbilicus was inverted, respiration, no scars, umbilicus was inverted,
no skin changes, No abdominal tenderness No no skin changes, No abdominal tenderness No
evidence of ascites. Bowel sounds were evidence of ascites. Bowel sounds were
difficult to appreciate difficult to appreciate
NEUROLOGICAL EXAMINATION
● Facioparesis
● Horizontal nystagmus
● Muscle wasting with fasciculation
● Flaccid quadriparesis
● Impaired joint position and vibration sense
● Global hypertonia and hyperreflexia
● Plantar responses absent
RESPIRATORY EXAMINATION
RR: 37 cycles/minChest wall is bilaterally symmetrical. No deformities or scars on the
chestChest expansion is equalTrachea is centralTactile fremitus and vocal resonance were
equal on both sides
Percussion notes were resonantBreath sounds were vesicular PresentlyRR : 24 cycles/min
INVESTIGATIONS
On Admission
Random blood sugar : 291mg/dl
Presently
Random blood sugar : 117mg/dl
INVESTIGATIONS
Full blood count
● White blood cells: 8.70 x 104 (4.00 -10.00)
● Neutrophils: 55.3% (40-60)
● Lymphocytes: 36% (20 -40)
● Hemoglobin: 13.1g/dl (12-16)
● Hematocrit: 40.2% (36-45)
● Platelets: 17.1 x 104 (15.7 -37.1)
INVESTIGATIONS
Computerized Tomography (CT) Scan
Pulmonary Angiogram (CTPA) showed emboli in the left main pulmonary artery
and segmented arteries (left & right).
ESR, EuCr, Viral markers, Urinalysis, HbA1C,.: which were normal
Cervical spine MRI
Lumbar Puncture for CSF analysis: cell count,biochemistry, cytology, virology,
MCS: which showed no presence of virus, slightly elevated glucose and protein
and a cytoalbuminologic dissociation that indicated a nerve root damage and is as
well as a supportive diagnosis of CIDP
DIAGNOSIS
MANAGEMENT AND TREATMENT
MEDICATIONS (WARD) MEDICATIONS (HOME)
● IV Methylprednisolone 1g in ● Tabs prednisolone 40 mg daily
100mls of normal saline to run ● Caps Omeprazole 40 mg daily
for 1 hr x5/7 ● Tabs calcium 600 mg daily
● IV Omeprazole 40 mg daily ● Tabs vitamin D3 0.25mg daily
● SC clexane 40mg daily ● Tabs Rivaroxaban 40 mg daily
● Tabs calcium 600 mg daily ● Physiotherapy
● Tabs vitamin D3 0.25mg daily
Chronic Inflammatory
Demyelinating
Polyneuropathy
(CIDP)
Outline
● Definition
● Overview
● Epidemiology
● Aetiology
● Pathogenesis
● Symptoms and signs
● Diagnostic tests
● Management and Treatment
CIDP (chronic inflammatory
demyelinating polyneuropathy) is a a
treatable immune‐mediated disorder of
Chronic Inflammatory
the peripheral nervous system and a
Demyelinating rare neurological condition that causes
Polyneuropathy worsening (progressive) muscle
weakness, numbness and abnormal
(CIDP) sensations in extremities of the body
that lasts atleasts over eight weeks.
OVERVIEW
Breaking down the name of the condition helps to understand it:
● Chronic: “Chronic” means “long-term.” CIDP slowly develops over at least eight weeks. It
can also improve and then come back (relapse) over the course of months or years.
● Inflammatory: Researchers think CIDP happens due to issues with your immune system,
specifically a type of autoimmune attack. This causes excessive inflammation that
damages your peripheral nerves— the nerves outside of your brain and spinal cord.
● Demyelinating: The inflammation specifically affects the myelin sheath of your nerves.
This is the protective sleeve (sheath) that’s wrapped around each nerve cell (neuron).
Demyelination refers to the destruction of the myelin sheath.
● Polyneuropathy: This is the malfunction of many peripheral nerves throughout your body.
“Poly-” means “many.” Neuropathy is the umbrella term for any kind of damage to your
peripheral nerves. Neuropathy can cause many issues, including muscle weakness and
abnormal sensations (paresthesia) like numbness
EPIDEMIOLOGY
Researchers estimate that there are 0.8 to 8.9 new cases of
CIDP per 100,000 people in the United States each year.
Approximately 30,000 individuals in the United States have CIDP.
This range is wide because CIDP can affect people in
many different ways and is difficult to diagnose because
of this.
CIDP can affect anyone at any age, but it more commonly
affects people assigned male at birth (AFAB).
AETIOLOGY
Researchers believe CIDP happens because of issues with your
immune system. For unknown reasons, your immune system sees
myelin as dangerous and attacks it (autoimmune reaction).
The myelin sheath is the protective layer around your nerve cells. It
wraps around the nerve axon — the long, wire-like part of a nerve cell.
Myelin allows electrical impulses to efficiently travel along your
nerves. When myelin is damaged or removed, it slows down or loses
these electrical impulses. And the “messages” may never reach their
intended destination. This causes the symptoms of CIDP.
PATHOGENESIS
The pathogenesis of Chronic Inflammatory Demyelinating
Polyneuropathy (CIDP) involves an immune-mediated
attack on the peripheral nervous system, leading to
progressive weakness and sensory dysfunction. The
underlying mechanisms are complex and involve both
cellular and humoral immune components.
● Immune Dysregulation:
CIDP is believed to be an autoimmune disorder, where the
immune system erroneously targets the peripheral nervous
system (PNS).
Triggers may include infections, vaccinations, or other
immune challenges, but the exact cause remains unclear.
● T-cell Mediated Immune Response:
T-helper cells (Th1 and Th17) become activated and release
pro-inflammatory cytokines (e.g., IFN-γ, TNF-α), which recruit
other immune cells to the nerves.
These cytokines lead to inflammation in nerve roots and
peripheral nerves, causing damage to the myelin sheath.
PATHOGENESIS
● Humoral Immune Response:
- Autoantibodies target specific components of peripheral nerves,
including myelin proteins (e.g., *P0, P2, or neurofascin*).
- Complement activation contributes to the demyelination process
and axonal injury.
● Macrophage Involvement:
- Activated macrophages invade the nerves and strip the myelin
sheath (macrophage-mediated demyelination), further impairing nerve
conduction.
Pathogenesis
● Demyelination and Axonal Damage:
- Loss of myelin results in slowed nerve conduction or conduction
block.
- Secondary axonal damage can occur over time, contributing to
long-term disability if untreated.
● Breakdown of the Blood-Nerve Barrier:
- Inflammation damages the blood-nerve barrier, allowing immune
cells and antibodies to infiltrate the PNS.
Symptoms
What are the symptoms of CIDP?
The symptoms of CIDP can vary based on the variant (type). The
classic presentation of CIDP is symmetrical weakness in both distal
and proximal muscles that progressively increases for a period of more
than 2 months.. It typically affects the muscles in the following areas
typically equally on both sides of your body:
Hips and thighs.
Shoulders and upper arms.
Hands
Feet.
Other symptoms of CIDP may include:
Loss of muscle mass (atrophy) in affected muscles.
Tingling, prickliness or numbness in your fingers and
toes (paresthesia).
Difficulties with balance and coordination (clumsiness).
In rare cases, you may also
Loss of mobility
experience:
Loss or weakening of deep tendon (muscle stretch)
Difficulty swallowing (dysphagia)
reflexes.
and weakness above your neck.
Neuropathic pain.
Double vision.
Variants of CIDP
Typical
Atypical Certain variants (types) of CIDP have different symptoms. Typical CIDP is the
most common form. It has symmetric (affecting both sides of your body) muscle weakness
and abnormal sensations (sensory symptoms).
Some atypical variants include:
● Multifocal motor neuropathy: This variant only causes muscle weakness. The
weakness is asymmetric, which means it affects different parts of your body.
● Lewis-Sumner syndrome: This variant has asymmetric muscle weakness and sensory
symptoms.
● Pure sensory CIDP: This variant involves numbness, pain, balance issues and an
abnormal gait (walking pattern). It doesn’t have muscle weakness as a symptom.
● Pure motor CIDP: This variant involves symmetric muscle weakness and loss of
reflexes but no sensory symptoms.
DIAGNOSTIC TESTS
● Electromyography (EMG) and nerve conduction tests: These tests evaluate the health and function of your
skeletal muscles and the nerves that control them. They specifically look for demyelination changes (like
slowing and blocks) in nerves to distinguish CIDP from the much more common types of polyneuropathy.
● Spinal tap (lumbar puncture): For this procedure, a needle is inserted into your lower back to get a sample
of cerebrospinal fluid (CSF). The sample sent to a lab where a pathologist examines the substances in it. In
about 85% to 90% of CIPD cases, there’s a normal amount of white blood cells and an elevated CSF protein
level. Other abnormalities in CSF may point to other conditions.
● MRI (magnetic resonance imaging) of your lumbar (lower back) spine: If nerve roots in your lumbar
spine pick up contrast dye as part of an MRI, it can support the diagnosis of CIDP.
● Blood tests: Certain blood tests are recommended to rule out other conditions that can cause neuropathy, like
diabetes, vitamin deficiencies, thyroid disease, Lyme disease, HIV or AIDS, lymphoma, and more.
● Nerve biopsy: In rare cases, may be recommend a nerve biopsy to look for evidence of demyelination.
MANAGEMENT AND TREATMENT
There are three go-to (first-line) treatments for CIDP, including:
● Corticosteroids: Prescription corticosteroids like prednisone can help improve inflammation. Many people see
improvement in their symptoms with corticosteroids alone. However, corticosteroids can cause serious side effects,
which limits how long you can take the medication. Your provider may also prescribe other medications, like those
that suppress your immune system (immunosuppressants), alongside corticosteroids.
● Plasma exchange (plasmapheresis): In this treatment, a machine separates the plasma from your blood, treats it, and
then returns the plasma and blood to your body. Plasma exchange filters out the antibodies in your plasma that are
attacking your nerves. Plasma exchange is typically only effective for a few weeks. You may need continued
intermittent (on-and-off) treatments over the course of months or years.
● Intravenous immunoglobulin therapy (IVIG): This treatment involves intravenous (IV) injections of
immunoglobulins, which are proteins that your immune system naturally makes to attack invading organisms. The
immunoglobulins come from a collection of thousands of healthy donors. IVIG can lessen your immune system’s
attack on your nerves. You may receive very high doses of IVIG initially and may need continued intermittent
treatments over the course of months or years.
● Physiotherapy sessions
LITERATURE REVIEW
● [Link]
● [Link]
● [Link]
hy
● [Link]
● Vallat JM, Sommer C, Magy L. Chronic inflammatory demyelinating polyradiculoneuropathy:
diagnostic and therapeutic challenges for a treatable condition. Lancet Neurol. 2010;9(4):402-412.
doi:10.1016/S1474-4422(10)70041-7
● Van den Bergh PYK, Hadden RDM, Bouche P, et al. European Federation of Neurological
Societies/Peripheral Nerve Society guideline on management of chronic inflammatory demyelinating
polyradiculoneuropathy: report of a joint task force of the European Federation of Neurological
Societies and the Peripheral Nerve Society - first revision. Eur J Neurol. 2010;17(3):356-363.
doi:10.1111/j.1468-1331.2009.02930.x
Typical
Typical CIDP is the most common form. It has symmetric (affecting both sides of your
body) muscle weakness and abnormal sensations (sensory symptoms).
Atypical
Multifocal motor neuropathy: This variant only Pure sensory CIDP: This variant involves numbness,
causes muscle weakness. The weakness is pain, balance issues and an abnormal gait (walking
asymmetric, which means it affects different parts of pattern). It doesn’t have muscle weakness as a
your body. symptom.
Lewis-Sumner syndrome: This variant has Pure motor CIDP: This variant involves symmetric
asymmetric muscle weakness and sensory symptoms. muscle weakness and loss of reflexes but no sensory
symptoms.
Researchers are currently studying other variants of
CIDP.