Clinical case 01

Disease stabilisation and functional improvement in primary lateral sclerosis

man, 47 · Kazakhstan

Small hand weights and a folded towel on a wooden bench by a clinic window

Patient record

Patient
man, 47
Country
Kazakhstan
Diagnosis
primary lateral sclerosis (PLS) – a motor neurone disease predominantly affecting the upper motor neurone
Duration
progressive course with increasing motor deficit
Main features
marked spastic paraparesis of the legs, weakness of the arms, muscle wasting, dysarthria, severely restricted walking
Previous investigations
Kazakhstan, Turkey, Germany
Treatment given
an individual combined cell, immunoregulatory and neuroregenerative protocol
Course after treatment
stabilisation, increased strength in the limbs, reduced spasticity, improved speech and sleep

History

The patient came to us with a progressive disease of the motor system, accompanied by a gradual increase in motor impairment.

By the beginning of 2024 his condition was already marked by a substantial neurological deficit. The medical records described tetraparesis, a pronounced pyramidal syndrome and signs of pseudobulbar involvement.

He had been investigated repeatedly, both in Kazakhstan and abroad.

At different stages of the diagnostic search several possible conditions were considered, including hereditary spastic paraplegia. Genetic testing was carried out to rule out Kennedy's disease.

He was then investigated further in Turkey and afterwards at a specialist centre in Germany. Following repeat clinical and electrophysiological examination, a diagnosis of primary lateral sclerosis was established.

Before coming to us the patient had been on symptomatic drug treatment, including medicines used in motor neurone disease and in marked spasticity, together with physiotherapy. Despite this, no substantial functional recovery was seen and the motor restrictions persisted.

Findings on examination

The neurological picture corresponded to predominant involvement of the central motor pathways.

On examination there were:

  • marked spastic paraparesis of the legs
  • reduced strength in the arms, mainly distally
  • considerably increased muscle tone of pyramidal type
  • brisk tendon reflexes
  • bilateral pathological pyramidal signs
  • muscle wasting
  • severely impaired walking
  • dysarthria

Stimulation electroneuromyography showed no significant involvement of the peripheral motor and sensory nerves examined.

Needle electromyography likewise showed no marked active denervation, which together with the clinical picture supported predominant involvement of the upper motor neurone.

Further specialist MRI revealed microstructural changes in the corticospinal tracts on both sides, that is, in precisely those pathways that carry voluntary movement.

At the time of the consultation

At the consultation the patient's main problems were:

  • marked weakness of both legs
  • considerable difficulty walking
  • mild distal weakness of the arms
  • marked spasticity
  • muscle wasting
  • impaired quality and clarity of speech
  • progressive loss of motor capacity

Given the nature of the disease, one of the main goals was to preserve as much as possible of the remaining functional reserve of the nervous system, to stabilise the patient's condition and to attempt to improve the functions already affected.

The programme

A combined regenerative and immunoregulatory protocol was designed for the patient, shaped by the clinical picture, the severity of the pyramidal syndrome and the predominant involvement of the central motor pathways.

At the first stage peripheral venous blood was collected to obtain the patient's own regulatory T lymphocytes, which were then cultured and prepared as autologous cell therapy.

The programme included:

  • mesenchymal stromal cells of placental origin
  • the patient's own autologous regulatory T cells
  • combined use of cell technologies
  • exosome therapy
  • additional neurotrophic support
  • a course of inhalation therapy
  • neurotherapy

Using several therapeutic directions made it possible to build a comprehensive programme aimed at once at immunoregulation, the neuroinflammatory component of the disease, trophic support of nerve tissue and preservation of the motor system's functional activity.

Course after treatment

At follow-up the patient reported a noticeable positive change.

One of the most significant developments was that the steady deterioration seen previously stopped progressing over the period of observation.

At the same time he noted functional improvements:

  • strength in the limbs increased;
  • spasticity became less marked;
  • movement came more easily
  • speech improved;
  • dysarthria became less pronounced
  • sleep returned to normal;
  • his general condition became more stable

The particularly important result was the combination of two processes: not only stabilisation of a previously progressive condition, but also positive change in motor and speech functions that were already impaired.

Outcome

This case shows what a personalised combined approach to complex neurodegenerative disease can achieve.

Before treatment began, we analysed in detail not only the wording of the diagnosis but the specific structure of the patient's neurological deficit, the level at which the motor system was affected and the functional reserve that remained.

On that basis an individual programme was built, bringing together cell technologies, the immunoregulatory direction, exosome therapy and methods of neurotrophic support.

As a result, after the programme the patient reported stabilisation, increased muscle strength, reduced spasticity, improved speech and normalised sleep.

For a patient with progressive involvement of the central motor pathways such a change matters a great deal, because it touches precisely those functions whose loss most determined his independence and the quality of his daily life.

This case is described from the patient's medical records and observation over the period after the programme. No personal data is published. The course of the disease and the response to treatment differ from patient to patient.

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