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How to diagnose and differentially diagnose young patients with acute leg weakness and subacute headache, irritation, paresthesia, sweating and urinary retention after infection? The clinical reasoning series of Neurology magazine reported a case of a 14-year-old boy with acute weakness, paresthesia and headache.
Let's take a look at the clinical reasoning process.
Edited by Yimaitong, please do not reprint without authorization.
Case brief introduction The patient is a 14-year-old boy with a history of atrial tachycardia and went to the emergency department due to acute weakness of his right foot.
One month before the treatment, the patient developed diarrhea and healed spontaneously; there was also bacterial pneumonia, which was cured by antibiotics.
After 2 weeks, the patient developed headache, irritation, and neck pain.
One week before the presentation, the patient developed intermittent urinary retention and flare-ups on the right face.
Five days before the consultation, the patient fell once, and in the following days bilateral hip pain and paresthesia gradually spread to both thighs.
On the day of consultation, the patient reported weakness in his right ankle and foot.
The patient denied fever, joint pain, swelling, skin rash, or facial paralysis, but was mildly sensitive to voice.
Nervous system examination showed normal mental state and normal cranial nerve function.
The Bruzinski and König signs were negative.
Muscle tone and muscle volume are normal.
The dorsiflexion, varus and valgus muscle strength of the right ankle was weakened (4/5), and the remaining muscle strength was normal.
The acupuncture sensation of the right leg was weakened, the joint position was normal, and the vibration sensation of the right ankle decreased.
Upper extremity reflexes are normal (2+), but bilateral Achilles tendon reflexes are absent (0), and bilateral knee reflexes are weakened (1+).
The mutual aid is normal, and the right foot is drooping.
Questions to ponder: 1.
Location diagnosis? 2.
What are the differential diagnoses? Localization and differential diagnosis of male adolescents after gastrointestinal and respiratory tract infections and acute right lower limb weakness and subacute headache, irritation, paresthesia, sweating and urinary retention.
Examination at the time of consultation showed that the right foot was drooping, reflexes were weakened, and vibration perception was weakened, but the mental state and cranial nerve function were normal.
Acute muscle weakness and weakened reflexes are localized to the lower motor neurons, and paresthesias indicate dorsal nerve root involvement.
Urinary retention and sweating indicate involvement of the autonomic nervous system and spinal cord.
Although not specific, headache, panic, and irritation suggest meningitis.
A single lesion is unlikely to explain the manifestations of polyneuropathy and myelitis.
The differential diagnosis of acute weakness and weakened reflexes includes trauma (such as spinal shock, acute nerve injury), side infections [such as acute inflammatory demyelinating multiple radiculopathy (AIDP)] and direct infection [such as polio virus, West Nile virus, acute flaccid myelitis (AFM)].
AIDP involves progressive (usually ascending) demyelination of peripheral nerves of motor and sensory fibers.
Cerebrospinal fluid (CSF) analysis is essential for the diagnosis of AIDP, because the protein level is elevated and the white blood cell count is normal.
AFM is limited to alpha motor neurons in the anterior horn of the spinal cord.
Therefore, by definition, there will be no sensory changes in AFM.
Involvement of the sacral cord usually has urinary retention.
If the ascending sensory tracts of the spinal cord are involved, a "sensory plane" can appear, but the patient has no sensory level.
Demyelination unrelated to infection is also possible, such as neuromyelitis optica (NMO), which has been tested for specific autoantibodies.
Finally, in endemic areas, Lyme disease that spreads early may cause multiple radiculitis or myelitis.
Questions to ponder: 1.
What diagnostic methods can be used to narrow the scope of differential diagnosis? How to narrow the scope of differential diagnosis? Neuroimaging and cerebrospinal fluid analysis can help narrow the differential diagnosis.
Pia mater enhancement can be seen in meningitis.
The T2 high signal of the spinal cord indicates myelitis, and the anterior horn edema can be seen in AFM.
The enhancement of cauda equina nerve root is an imaging sign of AIDP.
Cerebrospinal fluid cell increase is usually seen in direct infection, while AIDP can have protein cell separation (protein increase without cell increase).
Other tests to consider include serum Lyme and NMO Aquaporin-4 titer.
The patient’s head magnetic resonance imaging (MRI) showed high signal changes in the white matter T2 of the left parietal cortex, no enhancement (Figure 1A), and thickening and enhancement of the right trigeminal nerve (Figure 1B).
Spinal MRI showed a high signal change from T11 to cone T2 (Figure 1CD), and multiple cauda equina thickened and enhanced (Figure 1E).
The CSF analysis is consistent with bacterial meningitis: the red blood cell count is normal (15 cells/μl), the white blood cell count is increased (973 cells/μl; 84% of which are lymphocytes), and glucose is reduced (33 mg/dL) and Increased protein (178 mg/dL).
Cerebrospinal fluid culture and Gram staining were negative.
Lyme disease test is positive: IgM enzyme-linked immunosorbent assay (ELISA) is positive, while IgM 23 kDa, 39 kDa and 41 kDa Western blot bands are reactive.
CSF IgG index is normal, 1 CSF oligoclonal band, antinuclear antibody, myelin oligodendrocyte glycoprotein, or aquaporin 4 autoantibody are all negative.
Lyme disease seropositivity, CSF lymphocyte-based cells increased, and cranial neuritis, nerve root neuritis, and myelitis shown on MRI confirmed the diagnosis of early diffuse Lyme disease.
Figure 1 Patient imaging results.
A.
T2 FLAIR sequence shows the subcortical lesion (arrow) in the left parietal lobe, the lesion has no enhancement.
B.
T2 enhancement shows the thickening and enhancement of the right trigeminal nerve (CN V; arrow).
C.
Sagittal T2 spinal cord scan shows diffuse signal enhancement from T11 to cone (arrow). D.
Axial T2 shows patchy hyperintensity lesions of spinal cord gray matter with spinal cord edema.
E.
The T2 enhancement sequence shows the enhancement of multiple cauda equina nerve roots (arrows).
Questions to ponder: 1.
How to treat next? How to treat? Obtaining information about negative inspiration and vital capacity is especially important for patients with acute weakness and weakened reflexes.
The above tests in this patient were all normal.
While waiting for the examination, the patient received intravenous immunoglobulin (IVIG; 2 g/kg body weight; 5 days in a row) of hypothetical AIDP.
After 12 hours of hospitalization, the patient developed weakness on the right side of the face, and the forehead resolved within 48 hours.
Once the Lyme ELISA result was positive, intravenous ceftriaxone was started.
In view of the fact that steroids can aggravate the facial nerve palsy associated with Lyme disease, and intravenous antibiotics can improve the muscle strength of patients and resolve their urinary retention, so the treatment of methylprednisolone is postponed.
After the diagnosis of neuro Lyme disease was confirmed, the patient completed a course of IVIG, because it is reported that IVIG helps to improve the symptoms of early disseminated Lyme disease when the clinical features of AIDP are present at the same time.
Subsequently, the patient received 21 days of doxycycline therapy and was discharged from the hospital.
The follow-up 1 month after discharge showed that the right foot dorsiflexion was 5-/5, the knee reflex was 2+, the Achilles tendon reflex was (left 2+; right 1+), the paresthesia was completely relieved, and the patient was able to resume all normal activities .
Discussion The diagnosis of neuro Lyme disease is based on neurological involvement in endemic areas and positive serological results, with or without history of erythema migrans.
In a large study of patients with suspected neuro Lyme disease, 97% of patients had serum antibodies.
Among the remaining four serologically negative cases, only one was positive for CSF antibodies.
Therefore, serological double-layer detection (ELISA followed by Western blot detection) is often used clinically.
Lumbar puncture can be used to confirm whether patients with optic nerve head edema have elevated intracranial pressure and are therefore suspected of being pseudo-brain tumors.
Ceftriaxone or doxycycline is an antibacterial drug used for neuro-Lyme disease.
Acetazolamide can be used for pseudo-brain tumors associated with Lyme disease.
Borrelia burgdorferi infection can have different neurological manifestations.
Meningitis, cranial neuropathy, nerve root neuritis, and encephalomyelitis are all considered to be "early transmission" manifestations that occur weeks to months after infection.
Polyneuropathy is a late-onset symptom, usually a few months after infection.
In endemic areas, meningitis, cranial neuropathy and nerve root neuritis are the most common neurological complications of Lyme disease.
According to electromyography and nerve conduction examinations, the pathophysiology of the peripheral nervous system (PNS) associated with Lyme disease involves multifocal axonal injury.
Segmental myelitis secondary to Lyme disease occurs in less than 5% of cases.
As far as we know, this case is the seventh case of myelitis secondary to Lyme disease in a child, and the first case of myelitis associated with meningitis and radiculitis.
Although the pathophysiology has not been fully elucidated, human pathology studies have shown infiltration of plasma cells and lymphocytes in the white matter of the spinal cord.
Bai et al.
conducted experiments with infected rhesus monkeys, and the results showed that spirochetes were found in the spinal meninges, dorsal root ganglia, and motor and sensory spinal cord roots, but spirochetes were not observed in the spinal cord parenchyma.
This case suggests that the early diagnosis of Lyme disease is essential for the timely start of antibacterial drugs.
Especially in endemic areas, adult and pediatric patients with neurological symptoms that are not limited to a single lesion should consider neuro Lyme disease.
The neurological manifestations of early disseminated Lyme disease usually include meningitis, cranial neuropathy, and/or radiculopathy.
Encephalitis and/or myelitis are rare, but they can also occur. Original index: Ronald R.
Seese, Daniel Guillen, Jenna M.
Gaesser, et al.
Clinical Reasoning: A 14-year-old with acute weakness, paresthesias, and headache.
Neurology published online July 29, 2020.
DOI 10.
1212/WNL.
0000000000010088
Let's take a look at the clinical reasoning process.
Edited by Yimaitong, please do not reprint without authorization.
Case brief introduction The patient is a 14-year-old boy with a history of atrial tachycardia and went to the emergency department due to acute weakness of his right foot.
One month before the treatment, the patient developed diarrhea and healed spontaneously; there was also bacterial pneumonia, which was cured by antibiotics.
After 2 weeks, the patient developed headache, irritation, and neck pain.
One week before the presentation, the patient developed intermittent urinary retention and flare-ups on the right face.
Five days before the consultation, the patient fell once, and in the following days bilateral hip pain and paresthesia gradually spread to both thighs.
On the day of consultation, the patient reported weakness in his right ankle and foot.
The patient denied fever, joint pain, swelling, skin rash, or facial paralysis, but was mildly sensitive to voice.
Nervous system examination showed normal mental state and normal cranial nerve function.
The Bruzinski and König signs were negative.
Muscle tone and muscle volume are normal.
The dorsiflexion, varus and valgus muscle strength of the right ankle was weakened (4/5), and the remaining muscle strength was normal.
The acupuncture sensation of the right leg was weakened, the joint position was normal, and the vibration sensation of the right ankle decreased.
Upper extremity reflexes are normal (2+), but bilateral Achilles tendon reflexes are absent (0), and bilateral knee reflexes are weakened (1+).
The mutual aid is normal, and the right foot is drooping.
Questions to ponder: 1.
Location diagnosis? 2.
What are the differential diagnoses? Localization and differential diagnosis of male adolescents after gastrointestinal and respiratory tract infections and acute right lower limb weakness and subacute headache, irritation, paresthesia, sweating and urinary retention.
Examination at the time of consultation showed that the right foot was drooping, reflexes were weakened, and vibration perception was weakened, but the mental state and cranial nerve function were normal.
Acute muscle weakness and weakened reflexes are localized to the lower motor neurons, and paresthesias indicate dorsal nerve root involvement.
Urinary retention and sweating indicate involvement of the autonomic nervous system and spinal cord.
Although not specific, headache, panic, and irritation suggest meningitis.
A single lesion is unlikely to explain the manifestations of polyneuropathy and myelitis.
The differential diagnosis of acute weakness and weakened reflexes includes trauma (such as spinal shock, acute nerve injury), side infections [such as acute inflammatory demyelinating multiple radiculopathy (AIDP)] and direct infection [such as polio virus, West Nile virus, acute flaccid myelitis (AFM)].
AIDP involves progressive (usually ascending) demyelination of peripheral nerves of motor and sensory fibers.
Cerebrospinal fluid (CSF) analysis is essential for the diagnosis of AIDP, because the protein level is elevated and the white blood cell count is normal.
AFM is limited to alpha motor neurons in the anterior horn of the spinal cord.
Therefore, by definition, there will be no sensory changes in AFM.
Involvement of the sacral cord usually has urinary retention.
If the ascending sensory tracts of the spinal cord are involved, a "sensory plane" can appear, but the patient has no sensory level.
Demyelination unrelated to infection is also possible, such as neuromyelitis optica (NMO), which has been tested for specific autoantibodies.
Finally, in endemic areas, Lyme disease that spreads early may cause multiple radiculitis or myelitis.
Questions to ponder: 1.
What diagnostic methods can be used to narrow the scope of differential diagnosis? How to narrow the scope of differential diagnosis? Neuroimaging and cerebrospinal fluid analysis can help narrow the differential diagnosis.
Pia mater enhancement can be seen in meningitis.
The T2 high signal of the spinal cord indicates myelitis, and the anterior horn edema can be seen in AFM.
The enhancement of cauda equina nerve root is an imaging sign of AIDP.
Cerebrospinal fluid cell increase is usually seen in direct infection, while AIDP can have protein cell separation (protein increase without cell increase).
Other tests to consider include serum Lyme and NMO Aquaporin-4 titer.
The patient’s head magnetic resonance imaging (MRI) showed high signal changes in the white matter T2 of the left parietal cortex, no enhancement (Figure 1A), and thickening and enhancement of the right trigeminal nerve (Figure 1B).
Spinal MRI showed a high signal change from T11 to cone T2 (Figure 1CD), and multiple cauda equina thickened and enhanced (Figure 1E).
The CSF analysis is consistent with bacterial meningitis: the red blood cell count is normal (15 cells/μl), the white blood cell count is increased (973 cells/μl; 84% of which are lymphocytes), and glucose is reduced (33 mg/dL) and Increased protein (178 mg/dL).
Cerebrospinal fluid culture and Gram staining were negative.
Lyme disease test is positive: IgM enzyme-linked immunosorbent assay (ELISA) is positive, while IgM 23 kDa, 39 kDa and 41 kDa Western blot bands are reactive.
CSF IgG index is normal, 1 CSF oligoclonal band, antinuclear antibody, myelin oligodendrocyte glycoprotein, or aquaporin 4 autoantibody are all negative.
Lyme disease seropositivity, CSF lymphocyte-based cells increased, and cranial neuritis, nerve root neuritis, and myelitis shown on MRI confirmed the diagnosis of early diffuse Lyme disease.
Figure 1 Patient imaging results.
A.
T2 FLAIR sequence shows the subcortical lesion (arrow) in the left parietal lobe, the lesion has no enhancement.
B.
T2 enhancement shows the thickening and enhancement of the right trigeminal nerve (CN V; arrow).
C.
Sagittal T2 spinal cord scan shows diffuse signal enhancement from T11 to cone (arrow). D.
Axial T2 shows patchy hyperintensity lesions of spinal cord gray matter with spinal cord edema.
E.
The T2 enhancement sequence shows the enhancement of multiple cauda equina nerve roots (arrows).
Questions to ponder: 1.
How to treat next? How to treat? Obtaining information about negative inspiration and vital capacity is especially important for patients with acute weakness and weakened reflexes.
The above tests in this patient were all normal.
While waiting for the examination, the patient received intravenous immunoglobulin (IVIG; 2 g/kg body weight; 5 days in a row) of hypothetical AIDP.
After 12 hours of hospitalization, the patient developed weakness on the right side of the face, and the forehead resolved within 48 hours.
Once the Lyme ELISA result was positive, intravenous ceftriaxone was started.
In view of the fact that steroids can aggravate the facial nerve palsy associated with Lyme disease, and intravenous antibiotics can improve the muscle strength of patients and resolve their urinary retention, so the treatment of methylprednisolone is postponed.
After the diagnosis of neuro Lyme disease was confirmed, the patient completed a course of IVIG, because it is reported that IVIG helps to improve the symptoms of early disseminated Lyme disease when the clinical features of AIDP are present at the same time.
Subsequently, the patient received 21 days of doxycycline therapy and was discharged from the hospital.
The follow-up 1 month after discharge showed that the right foot dorsiflexion was 5-/5, the knee reflex was 2+, the Achilles tendon reflex was (left 2+; right 1+), the paresthesia was completely relieved, and the patient was able to resume all normal activities .
Discussion The diagnosis of neuro Lyme disease is based on neurological involvement in endemic areas and positive serological results, with or without history of erythema migrans.
In a large study of patients with suspected neuro Lyme disease, 97% of patients had serum antibodies.
Among the remaining four serologically negative cases, only one was positive for CSF antibodies.
Therefore, serological double-layer detection (ELISA followed by Western blot detection) is often used clinically.
Lumbar puncture can be used to confirm whether patients with optic nerve head edema have elevated intracranial pressure and are therefore suspected of being pseudo-brain tumors.
Ceftriaxone or doxycycline is an antibacterial drug used for neuro-Lyme disease.
Acetazolamide can be used for pseudo-brain tumors associated with Lyme disease.
Borrelia burgdorferi infection can have different neurological manifestations.
Meningitis, cranial neuropathy, nerve root neuritis, and encephalomyelitis are all considered to be "early transmission" manifestations that occur weeks to months after infection.
Polyneuropathy is a late-onset symptom, usually a few months after infection.
In endemic areas, meningitis, cranial neuropathy and nerve root neuritis are the most common neurological complications of Lyme disease.
According to electromyography and nerve conduction examinations, the pathophysiology of the peripheral nervous system (PNS) associated with Lyme disease involves multifocal axonal injury.
Segmental myelitis secondary to Lyme disease occurs in less than 5% of cases.
As far as we know, this case is the seventh case of myelitis secondary to Lyme disease in a child, and the first case of myelitis associated with meningitis and radiculitis.
Although the pathophysiology has not been fully elucidated, human pathology studies have shown infiltration of plasma cells and lymphocytes in the white matter of the spinal cord.
Bai et al.
conducted experiments with infected rhesus monkeys, and the results showed that spirochetes were found in the spinal meninges, dorsal root ganglia, and motor and sensory spinal cord roots, but spirochetes were not observed in the spinal cord parenchyma.
This case suggests that the early diagnosis of Lyme disease is essential for the timely start of antibacterial drugs.
Especially in endemic areas, adult and pediatric patients with neurological symptoms that are not limited to a single lesion should consider neuro Lyme disease.
The neurological manifestations of early disseminated Lyme disease usually include meningitis, cranial neuropathy, and/or radiculopathy.
Encephalitis and/or myelitis are rare, but they can also occur. Original index: Ronald R.
Seese, Daniel Guillen, Jenna M.
Gaesser, et al.
Clinical Reasoning: A 14-year-old with acute weakness, paresthesias, and headache.
Neurology published online July 29, 2020.
DOI 10.
1212/WNL.
0000000000010088
