No organ can make the body sick
Dinesh Kumar Jain in Homeopathy, 2022
Kent also said, “One organ cannot make another organ sick”. But the whole medical knowledge says that one damaged organ always damages the other organ. I am giving a few examples. Chronic obstructive lung disease is a disease of the lung. After sometime, this disease damages the heart, which is labeled as cor pulmonale. Cancer of one organ affects various organs of the body by metastasis. “Carcinoma in the kidney affects adrenal gland, bone, brain, heart, lung, liver, lymph node, ovary, pancreas, skin, spleen, thyroid gland and muscles” (Lee, 1976, p. 538). Similarly, cancer of many organs can affect other organs of the body. Disease of the pancreas gives rise to diabetes mellitus. Diabetes of prolonged duration damages the kidney, eye, and nervous system. Damage in the brain also causes damage to other organs of the body. Brain controls all functions of the body. Damage in the brain leads to hemiplegia, paraplegia, vision loss, speech loss, etc. Hemiplegia means paralysis of half of the body, and paraplegia means paralysis of both the lower limbs. Conclusively, Kent was again wrong in his observations.
Station 2: History Taking
Saira Ghafur, Parminder K Judge, Richard Kitchen, Samuel Blows, Fiona Moss in The MRCP PACES Handbook, 2017
On examination, this patient has signs suggestive of a spastic paraparesis. This is evidenced by hypertonia, hyperreflexia and decreased power throughout the lower limbs. There is tenderness over the T12 vertebra with a sensory level present, making spinal cord compression a likely cause. It is important to exclude acute spinal cord compression, so tell the examiners you would ask about bladder and bowel symptoms, and would offer to perform a pulmonary regurgitation (PR) examination.Always check gait and assess the functional status of the patient.
Post-viral syndromes
Avindra Nath, Joseph R. Berger in Clinical Neurovirology, 2020
Clinical features of TM are dependent on the level and cross-sectional area of the spinal cord lesion [25]. Sensory symptoms may include paresthesias (in 80%–95% of patients), numbness, and/or back pain (in 30%–50% of patients). A transverse sensory level can be seen in up to 80% of patients, most commonly in the thoracic region, though cervical and lumbar sensory levels are not infrequently seen. Paraparesis can be seen as well (in 50% of patients). Urinary retention (seen in almost 100% of patients) often necessitating bladder catheterization and constipation requiring aggressive bowel regimens are common as well. Deep tendon reflexes below the level of the lesion may be decreased or absent very early, however, typically become increased later on.
Depressed skull fracture compressing eloquent cortex causing focal neurologic deficits
Published in Brain Injury, 2023
Alexander In, Brittany M. Stopa, Joshua A. Cuoco, Adeolu L. Olasunkanmi, John J. Entwistle
Diffusion tensor imaging of patients with traumatic brain injuries suggests that motor weakness is most often caused by diffuse axonal injury in addition to intracerebral hemorrhage, transtentorial herniation, and focal cortical contusions (8). However, a depressed fracture fragment can rarely cause focal neurologic deficit(s) due to direct compression of the eloquent cortex (4–7). There are a few reports in the literature that have documented such phenomena (4–7). Mathew et al. (4) reported a case of a 26-year-old male who presented with acute onset isolated quadriplegia after an assault. Imaging demonstrated a midline biparietal depressed fracture with bilateral frontoparietal mixed-density lesions and surrounding edema suggesting venous infarction (4). CT venogram confirmed the injury of the superior sagittal sinus with a lack of filling within the middle one-third of the sinus (4). The patient underwent a biparietal parasagittal craniotomy, elevation of the depressed fracture, and repair of the superior sagittal sinus (4). At 6-month follow-up, the patient demonstrated marked improvement in neurologic function with MRC grade 4/5 power in all four extremities (4). Similarly, Syed et al. (5) described a case of a 55-year-old male who presented initially without neurologic deficits after an assault with imaging demonstrating a biparietal depressed skull fracture overlying the precentral gyri. One day later, progressive paraparesis was observed on examination; however, surgical intervention was not pursued (reason undisclosed) (5).
Genetic diseases mimicking multiple sclerosis
Published in Postgraduate Medicine, 2021
Chueh Lin Hsu, Piotr Iwanowski, Chueh Hsuan Hsu, Wojciech Kozubski
Common clinical presentations that AOKD shares with MS are spasticity, vision problems, numbness, weakness in extremities [76,77]. Spasticity affects approximately eighty percent of MS patients, making it the most disabling and frequent symptoms encountered in MS [78,79]. The most striking manifestations of transverse myelitis in MS are muscle stiffness, urinary dysfunction, sleep disturbances, and worsening mobility restrictions [79]. Wherein AOKD, musculoskeletal complications such as gait and weakness are often the first presenting symptoms. Paralysis ranging from paraparesis to tetraparesis is observed in the majority of affected individuals reported. Spasticity in AOKD results from damage to the cerebral cortex, and is mostly slowly progressive without a remitting period [80-83].
A new compound heterozygous mutation in adult-onset Krabbe disease
Published in International Journal of Neuroscience, 2020
Xianghe Meng, Yingjiao Li, Yajun Lian, Yujuan Li, Liyuan Du, Nanchang Xie, Cui Wang
Herein, we report a sporadic adult-onset case of KD with novel heterozygous mutations in GALC. The clinical manifestations of adult-onset KD are heterogeneous, and the late forms of the disease usually present with ataxia, muscle weakness, loss of vision, spastic paraparesis, behavioral problems, and dementia [14]. However, pyramidal involvement is a characteristic feature of the disease, with an incidence of such cases being 82-94% [3,15,16]. Our patient developed symptomatic onset at 40 years of age and demonstrated symptoms of typical paralytic paraplegia, such as weakness in the lower limb weakness, difficulty walking, increased muscle tone, and signs of pyramidal tract involvement, such as hyperreflexia and pathological signs. The extremely low activity of the GALC enzyme in the patient’s leukocytes and the presence of mutations in GALC led to a definitive diagnosis of adult-onset KD. The patient’s brain MRI showed signs of partial demyelination of the white matter, consistent with previously reported symptoms of patients with KD.
Related Knowledge Centers
- Birth Defect
- Lumbar Vertebrae
- Monoplegia
- Spinal Cord Injury
- Tetraplegia
- Thoracic Vertebrae
- Sacrum
- Motor Control
- Sensory Nervous System
- Spinal Canal